The patient: A 6-year-old boy in the Netherlands

The symptoms: The child was receiving a blood transfusion as a treatment for lymphoblastic leukemia, a type of blood cancer that originates in bone marrow, when he experienced a severe allergic reaction. His blood pressure dropped, and he developed a rash. Swelling appeared around his lips, tongue and eyelids, and he had difficulty breathing. This type of allergic response, known as anaphylaxis, can be life-threatening.

What happened next: Doctors treated the patient with the hormone epinephrine (also called adrenaline), which quickly reduces tissue swelling caused by anaphylaxis while also raising blood pressure and easing restricted breathing. The child recovered after about 30 minutes.

His doctors collected blood samples immediately after the reaction, and these contained unusually high levels of a type of protein called mast-cell tryptase, which is released by certain immune cells during anaphylaxis. However, the physicians were puzzled as to what had caused the extreme reaction, they wrote in a report of the case.

The diagnosis: The patient's mother told the doctors that her child had a similar allergic response to peanuts when he was about 1 year old, and since then, they'd omitted peanuts from his diet. The doctors then contacted the five blood donors who had provided the boy's most recent transfusion, and they learned that three of the five donors had eaten handfuls of peanuts the evening before they donated blood.

A protein in peanuts called Ara h2 is one of the main allergens that set off allergic reactions in people's immune systems. One of the building blocks of the allergen, called DRP-Ara h2, takes more than 24 hours to digest and remains capable of binding to receptors and triggering an allergic response throughout that time.

To see if this allergen could have played a role in the patient's reaction, the doctors performed another blood test that detects antibodies and is used for identifying allergic sensitivities. The test confirmed that the patient was allergic to peanuts and that antibodies against Ara h2 and DRP-Ara h2m were present in his blood post-infusion. These antibodies would have been produced in response to Ara h2 entering the bloodstream.

"These data are consistent with the hypothesis that the consumption of peanuts by the donors before blood donation provided the trigger for this patient's transfusion reaction," the doctors reported.

The treatment: The patient didn't require any further treatment after the epinephrine that was administered immediately to reverse anaphylaxis.

What makes the case unique: Allergic reactions during blood transfusions are rare, although estimates of their exact frequency vary. Some estimates suggest that they occur in about 0.001% to 0.006% of transfusions, while others find they occur in 0.1% of transfusions.

The triggers that set off these allergic responses are seldom identified. Prior to this case, other researchers suggested that blood transfusions could passively transfer food allergens from the donor to the recipient. Indeed, a growing body of evidence suggests that this may be more common than expected.

The child's response highlights the importance of identifying food allergies in people receiving blood transfusions, the child's doctors concluded, as well as the necessity of reviewing blood donors' recent diet histories to screen for potential allergens that could affect sensitive recipients.

"It is possible that allergens transferred in blood products to other patients have led to reactions that have gone unexplained and unreported," the doctors wrote in the case report.

This article is for informational purposes only and is not meant to offer medical advice.

Can you guess the diagnosis in these strange medical cases? Find out with our diagnostic dilemma quiz!

In the weeks around the 2026 annual meeting of the American Society of Clinical Oncology, my phone kept buzzing with alerts about GLP-1 drugs and cancer. The headlines were everywhere — from NPR and The Washington Post to Substack and heated exchanges on social media — all circling the same claim: Ozempic might lower the risk of cancer.

Behind those headlines is a real wave of studies, involving millions of patients. I'm a physician and clinical epidemiologist, and my team and I design and interpret these same kinds of studies that test what widely used drugs actually do.

The excitement around the idea that GLP-1 drugs can prevent cancer is running well ahead of the evidence. Not wrong, necessarily. Just not yet earned.

Cancer is among the hardest things to study, because it is not one disease but more than a hundred. Breast cancer, lung cancer and blood cancers are not variations of the same disease; each has its own distinct biology and its own mix of genetic, environmental and behavioral risks.

A single drug never gets one verdict on how it affects cancer. It gets a hundred, raising the risk of some, lowering it for others and leaving most untouched.

The early cancer concerns

Before the current buzz that GLP-1 drugs could reduce cancer risk, the worry ran in the opposite direction: that they might raise cancer risk.

Researchers were originally concerned about thyroid cancer. Studies in rodents found that Ozempic caused thyroid C cell tumors, which is why U.S. regulators added a black box warning in June 2026 to the drug that advises against its use among those with a personal or family history of related conditions.

But rodents are not people. Human thyroid C cells are less sensitive to GLP-1 drugs compared to rodent C cells because they have far fewer GLP-1 receptors. Long-term studies in monkeys did not show the same abnormal thyroid cell growth seen in rodents.

A 2025 analysis of data from 93 clinical trials found no clear link between taking certain GLP-1 drugs and thyroid cancer. European regulators reached the same conclusion in 2023 after reviewing available research on GLP-1s.

Pancreatic cancer was another concern. Here, too, researchers found no consistent increased risk from taking GLP-1 drugs in a 2025 analysis of data from 62 studies.

The reassurance is real but provisional. These drugs are young, and cancer can take decades to surface.

The cancer story turns on its head

GLP-1 drugs, once scrutinized for possibly causing cancer, are now being discussed as drugs that might prevent or even treat cancer.

A 2024 study of more than 1.6 million people with Type 2 diabetes found lower rates of 10 out of 13 obesity-related cancers in people treated with a GLP-1 drug compared to insulin.

A 2025 study of about 87,000 adults found that overall cancer rates among those who started a GLP-1 drug were roughly 17% lower, with the clearest reductions in endometrial and ovarian cancers as well as a type of brain cancer called meningioma. The risk of kidney cancer was 38% higher among patients taking GLP-1 drugs, though larger studies are needed to confirm its significance.

A 2026 study of more than 110,000 women undergoing breast imaging found a roughly 30% lower risk of breast cancer among those who use GLP-1 drugs compared to those who do not.

Researchers are also studying how GLP-1 drugs affect a patient's chances of surviving cancer. Among more than 6,800 colon cancer patients in a 2024 study, around 16% of the 103 on a GLP-1 drug died within five years compared to 37% of those who were not taking one. A study presented at the 2026 American Society of Clinical Oncology reported a 34% lower risk of death across six cancer types for those taking GLP-1 drugs.

Why the evidence is so easy to misread

While these findings are exciting, studies on the effects of GLP-1 drugs on cancer risk have three features that make them especially easy to misread.

The first is healthy user bias. People who start a GLP-1 drug tend to be healthier and wealthier than those who do not. A person with obesity who has insurance, sees doctors regularly and can afford Ozempic is far more likely to start the drug than someone with the same height and weight who lacks those advantages.

Healthy user bias is very difficult to scrub out of observational studies, which compare people as they are treated in real life rather than assigning the drug at random. The very advantages that made it possible to receive a GLP-1 prescription, not the drug itself, may be what lowered a patient's cancer risk.

The second is the choice of the comparison drug. To understand the effect of a drug, it has to be measured against something else. What it's measured against will shape the results of the study. The 2024 study reported that patients taking GLP-1 drugs saw large reductions in cancer risk compared to those taking insulin. But comparing patients on GLP-1 drugs with patients taking the diabetes drug metformin showed no clear reduction in cancer risk.

Insulin is reserved for patients with more advanced diabetes, a condition that is itself a risk factor for cancer. In these studies, patients on insulin start out with a higher risk of cancer. Measured against a group at higher risk of developing cancer, almost anything can look protective. The apparent benefit came from the comparison drug, not the GLP-1 drug.

The third is timing. It is not so much another source of bias as a clue that other biases may be at work. Cancer can take decades to develop, yet most GLP-1 studies follow people for only a handful of years. In some studies, the apparent cancer benefits of GLP-1 drugs show almost immediately. But prevention doesn't work that quickly. A drug that truly lowered the risk of developing cancer would show its effect gradually as fewer tumors surface over time, not within the first few months of taking a drug.

When cancer risk appears to drop almost as soon as a patient starts treatment, the speed is not a magical triumph of GLP-1 drugs. Rather, in my view, it is the tell: People who start these drugs were already at lower cancer risk, and the GLP-1 drugs are getting credit for that preexisting advantage.

Moreover, almost all of this research comes from a handful of high-income countries, even as uptake of these drugs is increasing globally and the burden of cancer has disproportionately grown in lower-income countries. The idea that GLP-1s may reduce cancer risk for much of the world is being inferred from data generated almost entirely in a few rich ones.

What do randomized trials show?

The cleanest way around these study biases is randomized trials, which by design make comparison groups alike from the start.

Available clinical trials tell a quieter story than the headlines. Two 2025 meta-analyses, which pool data from multiple studies — one covering 50 trials and a second covering 48 — found little evidence that GLP-1 drugs either raise or lower cancer risk.

The findings of these meta-analyses are generally more reliable than those of observational studies because their total amount of data increases their statistical power. Despite their strengths, these analyses inherit the limitations of the trials they include. Most of the trials in these 2025 studies had a short follow-up of a year or two and recorded too few cancer cases to settle the question.

Randomized clinical trials designed to answer the question of whether GLP-1 drugs affect cancer risk would need to enroll tens of thousands of people and follow them for many years. Short of that, the next best evidence will come from observational studies designed to emulate randomized trials.

Until then, the idea that GLP-1 drugs lower cancer risk is a hypothesis worth testing but not a conclusion to act on.

The bottom line

Based on the available evidence, the clearest conclusion is the reassuring one: GLP-1 drugs do not appear to raise overall cancer risk. However, more ambitious claims that GLP-1s actively prevent cancer or improve survival after diagnosis remain unproven.

Suppose GLP-1s do have an effect on cancer risk. Researchers still would not know where that effect comes from: weight loss itself, broader improvement in metabolic function, or a more direct effect on inflammation, the immune system or tumors.

The surest thing I can say is also the least satisfying: It's still too early. These drugs are far younger than the cancers they are being credited with preventing.

This edited article is republished from The Conversation under a Creative Commons license. Read the original article.

Younger generations may be aging faster than their predecessors, and this may be linked to a rise in early-onset cancers, a new study suggests.

There have been recent increases in the rates of some cancers among adults under 50, including breast, colorectal, kidney and uterine cancers. One 2023 paper suggests that these early-onset cancer diagnoses rose by 25% globally between 1990 and 2019, and scientists are still investigating why.

"The trend of increased cancers at younger ages is very real, and it is not simply because of more efficient diagnosis, or diagnosis at earlier stages," said Dr. Jyoti Nangalia, a hematologist and cancer researcher at the Wellcome Sanger Institute in the U.K. who was not involved in the new study. "It is possible that we are being exposed to new cancer-causing risks or that [our] defences to them are somehow altered," she told Live Science in an email.

The new study, published June 22 in the journal Nature Medicine, suggests that younger generations may have a wider "gap" between their chronological ages and their biological ages — a measurement of how quickly the body's tissues and systems are aging — than older generations do. The greater gap among younger adults seems to be linked with a higher risk of developing cancer early in life.

The new study cannot prove that faster biological aging causes early-onset cancer, but it provides new clues for scientists trying to unpack what might be driving the worrying trend.

"This is really proof-of-concept," study co-author Yin Cao, a molecular and clinical epidemiologist at the Washington University School of Medicine and Siteman Cancer Center, told Live Science.

Concerning trends lurking in dense data

Chronological age is straightforward: It's the number of years that have passed since a person's birth. "Biological age," however, can vary wildly from one person to another. This catch-all term describes a range of metrics, including markers on DNA and in the bloodstream. These are often measured using "aging clocks," which aim to determine if the body is acting much older than its chronological age.

Scientists have increasingly used these summary measures in an attempt to understand why some people are more prone to age-related diseases than others. To check whether there could be a link between biological age and the rise in early cancers, the new study analyzed data from more than 150,000 adults in the UK Biobank, a long-running project that has been tracking the health of about half-a-million U.K. adults since the mid‑2000s.

The participants had provided blood samples, with many already measured for markers used to track biological aging. The study authors plugged these results into PhenoAge, a statistical model that estimates a person's "age gap" at a given chronological age. In essence, this model can compare snapshots of two 40-year-olds — one born in 1950 and the other in 1965 — and see if their blood markers suggest they're the same biological age.

"The traditional approach is really focusing on individual risk factors" for cancer, such as a history of obesity or a high intake of ultraprocessed foods, Cao said. "We are testing whether we can leverage these large biobanks and potentially find some biological imprint as a potential reflection of many exposures that can be linked with cancer risk," she said.

The analysis revealed a concerning pattern: UK Biobank participants born between 1965 and 1974 had a larger age gap than those born between 1950 and 1954 at the same chronological ages. Based on PhenoAge's metrics, the younger cohort had systemic aging levels about 0.23 standard deviations higher than the older cohort — a modest shift toward older-looking biology.

The researchers applied this same approach to about 10,000 participants in the U.S. National Institutes of Health's All of Us Research Program, another large biobank. There, they found a more pronounced pattern: People born between 1990 and 1999 had age gaps about 0.92 standard deviations higher than those born between 1965 and 1969.

Another blood-based aging clock, called the Klemera-Doubal method, showed broadly similar patterns to PhenoAge, albeit slightly weaker ones, the study found.

Real trend or data mirage?

In the UK Biobank cohort, the researchers found that participants with higher age gaps were more likely to develop early-onset solid cancers, meaning cancerous tumors that appear in tissues, rather than "liquid" cancers present in bodily fluids. This link was strongest for lung, gastrointestinal and uterine cancers. This finding was based on the patients' medical records.

When the participants were divided into three groups based on their biological ages, those in the highest group had a roughly 15% higher risk of early-onset solid cancer than those in the lowest group.

To probe deeper, the authors used a different model that estimates biological aging at the level of specific organs and systems, using patterns of proteins in the blood. In almost 20,000 UK Biobank participants, they found that markers suggesting an "older-than-expected" immune system were linked with a higher risk of early-onset lung cancer. Similarly, markers suggesting older-than-expected fat tissue were linked with a higher risk of early-onset colorectal cancer.

Does this mean younger generations are aging faster and that's causing the rise in cancers? Maybe, but maybe not — there are important caveats to the study's findings.

The patterns will need to be confirmed in other datasets and populations, Cao noted. Biological aging tests, including PhenoAge, are also relatively new, and their implications aren't fully understood. While they clearly capture something about health and risk at the population level, at the individual level, different biological age tests can give very different answers for the same person. That raises questions about what any single score really means for individual health.

It may be that the differences PhenoAge uncovered between younger and older people have to do with how the test was originally calibrated, Stephen Burgess, a professor of biostatistics at the University of Cambridge who was not involved in the study, told Live Science in an email. To know if that's the case, one would have to dig deeper into how PhenoAge scores are calculated and see if that might have skewed its assessment of the UK Biobank and All of Us cohorts, he said.

Cao added that, while PhenoAge scores have been tied to mortality risk across a range of adults, the test "requires further validations" when it comes to assessing cancer risk.

As with any observational study using large databases, it is hard to untangle cause and effect, Nangalia added.

"The main issue for this paper is one of correlation versus causality," she said. "Either way, it is useful — with the first, as a potential way of tracking population health and cancer risk, and with the second, as insights into cancer-causing mechanisms."

Cao hopes her team's approach will serve as another useful tool to figure out why more young people are getting cancer. " Hopefully this is just a starting point," Cao said.

When the U.S. faces Paraguay in the World Cup in Los Angeles' SoFi Stadium on June 12, the teams will play on a natural-grass surface that, a month earlier, was carefully stitched together atop an underlying artificial-turf field. This "hybrid turf" installation was part of a broader effort in advance of the World Cup to ensure the world's best soccer teams played on predominantly natural-grass surfaces.

FIFA, the organization that oversees the World Cup, has prohibited the use of synthetic turf in World Cup games for years, mainly because of an increased risk of player injury, which has been well established. Synthetic turf is also notorious for causing nasty turf burns, as the material is a poor solar radiator and can reach up to 200 degrees Fahrenheit (93 degrees Celsius).

However, many people in the wider sports community worry that synthetic turf may pose more insidious harms, such as dangerous levels of exposure to heavy metals, cancer-causing chemicals and microplastics.

A recent, 10-year-long study from California found no significant risks from the chemicals in artificial turf. But experts aren't convinced the study has laid to rest concerns about artificial turf. Here's why.

Wonder of the Space Age

This infill is the crux of the issue: All those tire crumbs contain hundreds of chemicals and "created this exposure situation that had never existed previously," Rachel Massey, an environmental health researcher at the University of Massachusetts Lowell Center for Sustainable Production, told Live Science.

More than 95% of the 18,000 to 19,000 turf fields in the U.S. now include tire-crumb infills. AstroTurf has remained a dominant player offering 3G products. (Live Science reached out to AstroTurf to discuss the company's products but did not receive a response.)

Harmful chemicals?

Some researchers are concerned that turf contains nearly 400 chemicals that have been tied to various health risks, ranging from asthma to leukemia.

"None of those [risk assessment] studies dispute the fact" that those chemicals are present, Massey said. "So then all the debate is about exactly how much exposure there is."

To assess whether that exposure reached harmful levels, the California Office of Environmental Health Hazard Assessment (OEHHA), part of the California Environmental Protection Agency, undertook a study of the health impacts of chemical exposure due to synthetic turf.

"We identified as many chemicals as we could in the crumb rubber by doing non-targeted sampling and assessed as many chemicals as we could," said Amy Gilson, a spokesperson for the OEHHA.

They attempted to measure exposure to metals commonly found in turf infill, including lead, cadmium, manganese and zinc, with zinc being most frequently detected at concerning levels above U.S. regulatory guidelines. Although zinc is essential to the body, it can be harmful at high levels, with the potential to cause anemia, damage the pancreas, and reduce fertility.

They also looked at carbon black, a reinforcing tire filler material that has been shown to kill human cells in lab dishes; benzene, which has been linked to several types of leukemia; toluene, which is toxic to the nervous system, liver and kidneys; and polycyclic aromatic hydrocarbons, compounds that are most commonly found in tobacco and wood smoke and have been tied to cancer in animal studies.

Another potential concern emerged last year, when 1,3-dimethylbutylamine (1,3-DMBA), a stimulant banned by the World Anti-Doping Agency, was detected in post-match samples submitted by eight Norwegian female professional league soccer players from opposing teams. The artificial turf was found to be the source of the banned substance. With tire wear, 6PPD ‪—‬ a substance often added to tires to limit ozone-depleting emissions ‪—‬ can degrade into 1,3-DMBA, which was detected on the turf where the game was played.

The California EPA report also looked into the presence of microplastics in turf.

In 2023, the European Union announced a ban on the sale of products containing intentionally added microplastics, effective starting in 2031. Specifically, it named the granular infill within artificial turf as "the largest source of intentional microplastics in the environment." The U.S. does not have similar legislation.

Microplastics might harm human health by accumulating in various parts of the body through ingestion, skin contact or inhalation.

Early research in human cells in lab dishes hints that microplastics could damage the lining of blood vessels and promote the formation of atherosclerotic plaques and blood clots. Other studies have proposed potential links between microplastic exposure and asthma and inflammatory bowel disease. However, there is a lot of uncertainty about how microplastic exposure is measured and whether this exposure causes diseases or is simply a proxy for some other factor that causes these conditions.

"Negligible" long-term harm

The California EPA focused on chemicals in tire infill that could potentially cause harm at high doses. Then, it estimated the levels of exposure in players, referees and spectators through having direct contact with, breathing in, or inadvertently swallowing tire crumbs. First, they estimated exposure indirectly, by observing people.

"We actually had teams of people going out and videotaping players on the field," Gilson said.

The research team also collected samples of artificial turf and then put them in lab dishes with synthetic bodily fluids such as sweat, saliva and small intestine fluid and then measured the concentrations of dozens of potentially harmful chemicals within those fluids. To be more conservative, they assumed every chemical detected in their experiments would have been completely taken up by human cells, Jocelyn Claude, a toxicologist at the OEHHA who worked on the study, told Live Science.

The study found "no acute risks," meaning short exposure to this substance is unlikely to cause immediate harm, she said, and the risks of longer-term health effects, such as cancer or reproductive harm, "were negligible."

But some experts said the study methodology was flawed. Andrew Watterson, a professor emeritus of public health at the University of Stirling in the U.K., said the study should have taken urine or expelled-air samples directly from real people exposed to artificial turf, instead of estimating exposure in synthetic body fluids.

Wrong approach to risk assessment

For Massey and several environmental researchers Live Science spoke to, the bigger problem is that the underlying approach used by the California study — and most other environmental assessments done in the U.S. — is flawed.

Instead of asking whether an average person is at risk, society should aim to reduce exposure across the population, which also protects people at higher risk. Instead of asking, "Is this risk acceptable?" the latter approach asks, "How can we create the healthiest, safest playing surface for a child?" Massey said.

The California report included referees and spectators in addition to players, but it may have missed other at-risk groups, such as people exposed to chemicals that have leached into the water supply from synthetic turf, said Tracy Stewart, a Medway, Massachusetts resident who advocates against the use of artificial turf.

Another byproduct of 6PPD, the chemical tied to doping, has been shown to cause mass die-offs of coho salmon. So when dead salmon started turning up near an artificial turf field in Vancouver where scientists had detected 6PPD-Q and a range of other chemicals in the stormwater runoff, the community was worried.

The California study estimated 6PPD-Q exposure levels in synthetic bodily fluids, but it did not model how groundwater would be affected. And without well-established safe limits for this chemical, the California study couldn't make assessments of the risk it poses.

Beyond 3G turf

The attraction of synthetic turf is all about "increased hours of use," said Garnet Brownbill, a spokesperson for the Natural Turf Alliance, a nonprofit that advocates for alternatives to synthetic turf across Australia. "It's not impacted by the weather, it never closes, and people claim it's maintenance-free — it's not, by the way," he told Live Science.

However, in response to the looming EU ban on microplastics in infill, many scientists are working on alternatives that can provide that same advantage.

One material in development is hybrid turf, whose surface is "99.5% natural grass," with an additional 0.5% stitching material composed of either plastic or a biodegradable polymer, said Aaron Golembiewski, head of business development at Turftalents, a company that consulted for FIFA on the installation of hybrid turf at several U.S. stadiums. Hybrid turf is "stronger than if it's grass alone," Golembiewski told Live Science. "It increases [the] quantity of play."

It's also smoother than ordinary grass, which has naturally occurring bumps and divots. He noted that hybrid turf is cheaper to install from scratch than synthetic turf and lasts a few years longer, although it needs more maintenance.

Grass fields may be sufficient for many communities. While some stakeholders figure out how to maintain grass more sustainably, other scientists are working to improve the grass itself. "If the same amount of engineering went into natural grass, there's all of this stuff that we can do," Brownbill said. Not all grass is the same.

"There are high-heat-resilient grasses; there are shade-resilient grasses; there are high-wear grasses," Brownbill said. "[Municipalities] are basically using 100-year-old technology … the same grass cultivars that existed 100 years ago."

Editor's Note: This article was produced as part of the Dalla Lana Fellowship in Journalism and Health Impact program at the University of Toronto.

How much do you know about the greatest athletic feats of all time? Find out with our sports record quiz!

Emerging diagnostic tests for cancer aim to detect the disease in its earliest stages, to improve patients' chances of survival by enabling earlier treatment. Some of these diagnostics — called multi-cancer early detection (MCED) tests — screen for many cancers at once, which sounds great on paper.

However, in February, a flagship trial testing one such cancer test, called Galleri, failed to meet its primary endpoint: it didn't reduce the number of late-stage cancer cases identified. In May, at the American Society of Clinical Oncology (ASCO) meeting in Chicago, attendees got a closer look at some of the data behind the trial.

The trial was the biggest of its kind in the field to date and its high-profile failure drew a lot of attention. But experts told Live Science that it doesn't mean we should count out MCED technology.

Why Galleri was put to the test

The majority of cancer diagnoses and deaths are from cancers that have no well-established screening program, such as pancreatic cancer. Without these early-detection methods, like regular colonoscopies for colorectal cancer, many cancers are caught late.

The perfect MCED test could, in theory, make finding cancer a breeze. Such a test could use a single blood sample to screen for many cancers, detecting disease-linked changes in DNA and other cellular markers of disease floating in the bloodstream.

But designing a trial that proves that MCEDs can improve patient outcomes is difficult. Earlier diagnosis can be life-saving in some types of cancer, said Jessica Lloyd, a strategic evidence manager at the nonprofit Cancer Research U.K. Five-year survival rates drastically improve when lung or colorectal cancer are detected at an earlier stage. But for other cancers, such as melanoma, earlier diagnosis makes little difference to overall survival rates.

The ideal trial would follow a group of patients over many years; one half would receive MCED testing while the other would not. At the end of the trial, data would reveal whether overall cancer deaths were reduced in the group that received testing.

But there's already a lot of hype around MCED tests, and there's little appetite in the field to wait years for clear results that the tests improve outcomes, or to pay the high price tag that such long studies would incur.

Instead, the recent trial of Galleri, run in collaboration with the U.K.'s National Health Service (NHS), lasted only three years. It measured whether the test could identify cancers at an earlier stage, considering the early detection a proxy for mortality data. In other words, early detection was assumed to lead to lower death rates.

The trial recruited 142,000 healthy people ages 50 to 77. Participants had their blood drawn roughly once a year for three years. Each time, for a subset of participants, the Galleri test looked for markers linked to 12 different types of cancer. If a patient tested positive, they received further treatment. This tested group was compared to another that didn't have their blood tested.

The aim of the trial was to assess whether significantly fewer cases of late-stage cancers — meaning stages III and IV — would be detected in the test group; at that stage, disease has started spreading beyond the cancer's origin point to other tissue. The rationale was that the test would instead pick up these cancer cases in stages I and II, before the disease had spread. But Galleri failed to meet this endpoint.

Samantha Harrison, Lloyd's colleague and head of strategic evidence at Cancer Research U.K., said that the test's failure to reach its main target is "disappointing." However, she added that the trial's huge dataset hasn't been detailed in a peer-reviewed publication yet, which would shed more light on the trial's full value.

What went wrong for Galleri?

Galleri's problems were related to both the diagnostic test itself and the trial design, said Ruth Etzioni, a biostatistician at Fred Hutchinson Cancer Center in Seattle. Galleri caught an unexpected number of advanced cancer cases among the trial volunteers the first time they were tested.

These cases came as a surprise, because the volunteers recruited to the trial had not been diagnosed or treated for cancer over the previous three years. Etzioni said that if the trial were begun anew, these initial cases would likely be excluded from the analysis, which would have helped improve Galleri's performance.

But even with that adjustment, she added, it's unlikely the trial results would have significantly changed. That's because the test was unexpectedly bad at picking up early-stage cancer, she told Live Science.

"That's critical," she said. "You have to have an increase in stage I to II, and then that then coincides with the decrease in stage III to IV," she said.

The MCED test doesn't look for a lone marker that determines whether a patient has cancer or not. Instead, the various disease markers that the test looks for are weighed and a threshold is applied, above which the test yields a positive result. Etzioni said the test appeared to be conservative in how it registered these positive results; it applied a high threshold to deem a case "positive." That may explain why the harder-to-detect, early-stage cancer cases were not picked up.

But she added that some of the more dismissive commentary around Galleri's performance is "short-sighted."

"I don't think that this trial was a flop," she said. "I think it was hugely informative."

Galleri hopes that results from its upcoming Real-world Evidence to Advance Multi-Cancer Early Detection Health Equity (REACH) study, which has enrolled 50,000 patients in the U.S., will be more positive. The REACH trial has a slightly different endpoint in that it's measuring the test's ability to reduce stage IV diagnoses. The data from the NHS trial suggested Galleri did reduce these diagnoses, which was a secondary endpoint of the trial.

What does this mean for other MCED tests?

Galleri is just one of many MCEDs under development. What could the negative results from Galleri's initial trial mean for the future of cancer detection?

MCED tests are proliferating rapidly, and improvements to the panels used to detect cancer markers should enhance the performance of newer tests, said Etzioni. That said, she noted that, as these tests are closely guarded by manufacturers, it's hard to know exactly which markers would advance performance. Dozens of presentations at ASCO 2026 focused on other MCEDs in the field.

Galleri's results might mean a slightly longer wait before the tests are used widely, Etzioni said. She felt that some of the hype from GRAIL's earlier studies of the test has now dissipated. "They've maybe [previously] led the community to believe that the technology is more ready for prime time than it actually is," she suggested.

Harrison pointed to a position statement from the U.K. National Screening Committee (UK NSC), which provides advice to government ministers on implementing new disease screening programs. The statement, released in May, directly addressed so-called surrogate endpoints, such as the cancer stage-related endpoints used in the initial Galleri trial.

One concern, it pointed out, is that MCED tests may more easily detect aggressive cancers than slow-growing ones. So even if future trials show the tests find these cancers at earlier stages, patients may still die at similar rates because the types of cancer found at these early stages are harder to treat. So improvements in detection can't be assumed to translate to improvements in survival.

The UK NSC stated that further evaluation would likely be required before a MCED test would be adopted in widespread clinical practice, such as within the NHS. (For what it's worth, though, some MCEDs are available for direct-to-consumer purchase despite not proving their worth in gold-standard trials yet.)

The Galleri trial focused on the test's ability to identify cancer in a (presumably) healthy population, but this is just one potential use of the technology behind the tests. It could also be deployed to test people with non-specific symptoms that may hint at cancer or in populations who are known to be at high risk of the disease. Another NHS Galleri trial, called SYMPLIFY, suggested the test was accurate when used in symptomatic patient groups, Lloyd noted.

Galleri's results are not a reason to discount the value of MCED tests more widely, Etzioni said. She believes the tests will someday be used routinely for early cancer detection.

"This is just the beginning," she said.

This article is for informational purposes only and is not meant to offer medical advice.

The first-ever whole-genome sequence of a Greenland shark has revealed genetic clues to how the animals avoid cancer and live for hundreds of years. The work may pave the way to a better understanding of age-related diseases in humans.

Greenland sharks (Somniosus microcephalus) typically grow to about 13 to 16 feet (4 to 5 meters) and live long lives in the North Atlantic and Arctic oceans. Little is known about these sharks, partly because they live at depths of up to 1.65 miles (2.65 kilometers). They are estimated to live to about 400 years and don't reach maturity until they're about 150 years old, making them the longest-living vertebrates in the world.

Now, new research by Shigeharu Kinoshita, a fisheries chemist at the University of Tokyo, and his colleagues has uncovered nearly the entire sequence ‪—‬ 96.7% ‪—‬ of a Greenland shark genome. In their study, published May 19 in the journal PNAS, the researchers found a wealth of genes that could be linked to the sharks' longevity.

Key among the findings were genetic tweaks relating to unique amino acid substitutions in "linker histone proteins," a series of proteins that spool and compact DNA. These changes may stabilize the structure of the sharks' chromatin, the mixture of DNA and proteins that makes up the chromosomes. This, in turn, may help to suppress the accumulation of DNA damage over the sharks' exceptionally long lifespans, Kinoshita told Live Science by email.

The researchers also found that gene families related to immune responses and DNA repair pathways were expanded in the shark genome. This finding, Kinoshita said, supports the idea that efficient damage repair and regulation of the immune system are key components of both longevity and cancer resistance.

A third discovery that provides clues to the sharks' longevity was the marked expansion of ferritin genes, which are involved in iron storage and regulation. This gene expansion suggests the sharks have a boosted capacity to control iron metabolism and to limit oxidative stress, which can damage DNA and lead to cancer. It may also mean they restrict a mechanism called ferroptosis, an iron-dependent form of programmed cell death.

"Our genomic analyses revealed multiple lines of evidence pointing to enhanced genome stability and stress resistance in the Greenland shark," Kinoshita said. "Extreme longevity is likely governed not by a single gene, but by coordinated changes across multiple biological systems, including genome stability, iron metabolism, immune function, and stress resistance," he said, adding that the work could inform research on human aging and age-related diseases.

The features linked to immune enhancement, cancer resistance, DNA repair and chromatin stability may help to explain the shark's extreme lifespan, said Dorota Skowronska-Krawczyk, a physiologist and biophysicist at the University of California, Irvine, who recently showed how DNA-repair-associated genes in the retina may help keep the Greenland shark's eyesight clear over its long life. "This could be related to longevity and cancer resistance, but functional studies will be needed to test that idea directly," said Skowronska-Krawczyk, who was not involved in the research.

Previous work suggested that the sharks' metabolism remains stable throughout their lives, which has been given as another reason for their epic longevity.

Aaron MacNeil, a biologist at Dalhousie University in Nova Scotia who was not involved in the research, told Live Science that the results support the idea that the sharks are particularly long-lived. But MacNeil is skeptical of the 400-year age estimate, which is based on radiocarbon isotope traces left over from Cold War nuclear bomb testing seen in the eyes of sharks. The eye lenses grow in layers, so seeing where the isotope sits in the layers gives a fixed point in time that helps assess the animals' age.

The slow mixing of different layers of the ocean in the cold depths where Greenland sharks live means it could take longer for the bomb radiocarbon to reach the deep sea, and thus the age estimate for the sharks may be too high. "But we do know they're damn old — 200 years at least," MacNeil said.

How much of a shark fan are you? Find out with our shark quiz!

A common asthma drug could be repurposed to help tackle hard‑to‑treat cancers, such as triple‑negative breast cancer, an early study suggests.

The research finds that cysteinyl leukotriene receptor 1 (CysLTR1), a protein found on many cells, may be hijacked by tumors to turn important immune cells into sleeper agents that work for the cancer instead of against it. Those immune cells, called neutrophils, would normally directly kill tumor cells, help to rally other immune cells against cancer, or boost the effects of certain cancer therapies.

However, research increasingly suggests that the cells are an important player in how cancers resist immunotherapy. Under certain conditions, they help build and maintain a tumor-promoting environment.

If the new study's finding is confirmed in future research, an existing medication could offer a way to target this receptor and thus reverse cancers' resistance to common immunotherapies. There's already a drug on the market that can block CysLTR1, called montelukast, which has historically been used to treat asthma and allergies.

The work suggests that "you can repurpose these drugs to revive or to reprogram those neutrophils to become immune stimulatory cells that basically sensitize tumors to immunotherapy," study co-author Dr. Bin Zhang, a professor of cancer immunology at Northwestern University Feinberg School of Medicine, told Live Science. The research, published Tuesday (May 19) in the journal Nature Cancer, could also help to explain why some patients don't respond to immunotherapy, a treatment that redirects the immune response toward cancer cells.

"There are not many options available for patients who are resistant [to immunotherapy]," Zhang said. "But now, using this drug, it seems like they [could] start to respond to the treatment."

Immune cells called to the dark side

CysLTR1 is an important actor in immune responses; it helps recruit immune cells to a site of infection and prompts the lungs to produce mucus and cough out any invading microbes, for instance.

The problem comes when that reaction gets out of hand. In asthma, blocking CysLTR1 can do wonders, alleviating symptoms like wheezing, breathlessness and allergy‑related nasal symptoms. The drug montelukast does just that, and it has been approved by the Food and Drug Administration (FDA) since 1998 to treat asthma and hay fever.

The new research suggests that CysLTR1 can also be co‑opted by tumor cells to cause neutrophils to adopt "tumor‑promoting" behavior. By releasing chemicals that tweak the behavior of immune cells — cytokines and cysteinyl leukotrienes — tumor cells encourage neutrophils to release powerful molecules that help cancer cells invade surrounding healthy tissue. They also help tumors ward off attacks from other immune cells that would normally seek out and help kill cancerous tissue.

"We identified this molecule plays a very important role in controlling neutrophils, which is one of the most abundant immune populations in the circulation, particularly in cancer patients," Zhang said.

When researchers blocked CysLTR1 in lab mice, by either turning the gene off or using montelukast, they found that they could slow tumor growth, increase the mice's survival time, and make previously resistant tumors respond better to immunotherapy drugs.

Blocking CysLTR1 worked across several tumor types in mice, including breast, colon and melanoma‑like cancers. It was particularly strong when combined with a common type of immunotherapy called "checkpoint blockades," causing once-resistant tumors to shrink under treatment.

This is important because some cancers, such as triple‑negative breast cancer, don't tend to respond well to checkpoint blockades, Zhang said. At least from preclinical models, we suggest that when checkpoint blockades and montelukast are combined together, "you see beautiful results reflected by increased survival" across multiple tumor types.

"It's a very amazing result," he said.

Turning science into treatment

In experiments with human cells, the team found that blocking CysLTR1 in human blood reduced neutrophils' ability to shut down cancer‑killing immune cells. It also stopped neutrophils from maturing into this tumor‑helping, immune‑suppressing state, suggesting that the same pathway the team saw in mice is also active in people. Using a genetic analysis, the team unraveled the chain of events that CysLTR1 triggers to switch into this "cancer-promoting" mode.

They then uncovered clues that this same mechanism had left traces in large cancer datasets. They found that patients whose tumors had more of the receptor tended to do worse overall and responded less well to checkpoint blockades.

Shakti Ranjan Satapathy, a postdoctoral researcher at Lund University in Sweden who studies this field but was not involved in the new research, said the study was "important and timely" and "moves the field forward."

Zhang is hopeful that the team will be able to launch a clinical trial on the back of their results."It's not easy, sometimes, doing a clinical trial, but in this case, it may be a little bit less challenging because those drugs are available," he said.

The team also suggests that doctors screen for this receptor to determine whether patients are likely to resist immunotherapy. "We are probably the first to demonstrate [CysLTR1 as] maybe a functional biomarker that could be linked to the patient prognosis and help predict the immunotherapy resistance," Zhang said. Still, there is a lot to be tested before this drug can be confidently rolled out in the context of cancer, he said.

"'Quickly move into trials' should not be confused with 'ready for routine cancer treatment,'" Satapathy cautioned. "Repurposing an approved drug still requires an appropriate dose, dosing schedule, patient selection strategy, safety monitoring, pharmacodynamic readouts, and evidence of benefit in combination with immunotherapy."

For one, montelukast is occasionally linked to substantial neuropsychiatric side effects when used for hay fever, including suicidal thoughts and mood changes, leading the FDA to raise a boxed warning in 2020. One alternative, Zhang said, might be to test whether the receptor could be targeted directly with an antibody, which could potentially cause fewer side effects, rather than a chemical, though further research will be needed to assess if this is the right path.

"Hopefully, we can have a real clinical impact," he said, "but that's too early to say."

This article is for informational purposes only and is not meant to offer medical advice.

The patient: A 59-year-old woman in Wisconsin

The symptoms: The woman sought medical care after noticing a rapidly growing mass in her right arm.

What happened next: Upon examination, doctors found a 0.8-by-0.8-inch (2 by 2 centimeters) mass in the patient's forearm that was firm to the touch. The mass could also be seen on an X-ray of the woman's arm, and the roughly oval-shaped lump appeared bright white on an MRI scan. This finding hinted that the mass might be a sarcoma, a type of cancer that starts in bone or soft tissue, such as cartilage, fat or muscle. Sarcomas are relatively rare; they make up only about 1% of cancer diagnoses.

To further examine the lump, doctors performed a core needle biopsy, which involves inserting a small, hollow tube into the tissue to collect a sample. They also collected fine needle aspirates, or biopsies of cells and fluids collected using a small needle and syringe.

The diagnosis: Analyses of the biopsied samples showed that the woman had myxofibrosarcoma (MFS), a type of cancer that develops in connective tissues beneath the skin, often in the limbs. MFS cases make up about 5% to 10% of soft tissue sarcomas; a few hundred new cases occur in the U.S. each year.

The cancer cells in the woman's biopsy were classified as Grade 2, or intermediate grade; in terms of the abnormality of the cells and expected speed of tumor growth, the cells were a 2 on a scale of 1 to 4, with 4 being the most abnormal and fastest growing.

The treatment: Following her biopsy, the patient reported that the mass in her arm had suddenly begun to shrink, and in two weeks, it could no longer be felt through her skin. Although the mass seemed to have disappeared, her medical team performed a procedure to remove the tissue where the lump had been "to ensure disease control," doctors wrote in a report describing the case.

They performed a wide local excision, meaning they removed tissue from the tumor site and a bit of healthy tissue surrounding it, to help prevent regrowth. However, the team spotted no viable cancer cells in the tissue they removed. The tissue showed scarring and inflammation that might be expected following an anti-cancer immune response, but the cancer itself had gone.

One year later, the patient remained cancer-free, the report said.

What makes the case unique: The woman experienced what's known as a spontaneous regression of malignancy, meaning the partial or complete disappearance of cancer without any treatment. Spontaneous regression can also sometimes occur after a patient receives a treatment that wouldn't be expected to effectively shrink a cancerous tumor.

Spontaneous regression is rare across all cancer types, but given that sarcomas are rare at baseline, there aren't many published descriptions of the phenomenon. In their report of the woman's case, which was published in April, the doctors found 32 previous reports of spontaneous regression of malignancy in sarcomas, including nine involving MFS.

Of the 32 cases of spontaneous regression, eight (25%) began after a diagnostic biopsy or some other physical trauma to the tumor, they found. Infections, such as pneumonia, appeared to be the trigger in three cases, and for most of the remainder, a specific trigger couldn't be identified.

The median time from biopsy to regression in these biopsy-triggered cases was less than a month. Regression due to infections had a median response time of five months, while the others regressed in about three months.

Half of the biopsy-associated cases saw complete tumor regression, while the others had near-complete or partial regression. Surgical resection was still performed in most of the cases, with some patients showing no signs of cancer cells in the resected tissue and others having some lingering cells.

The report authors hypothesized that physical disruptions to the tumor's structure during a biopsy releases tumor-related proteins into circulation that can then be spotted by the immune system. Simultaneously, the biopsy summons immune cells to the tissue by triggering a wound-healing process.

This chain of events may expose the tumor to the immune system while also spurring a local immune reaction at the tumor site. The scarring and inflammation evident in the patient's resected tissue may support that hypothesis.

That said, "the observation of a regressing sarcoma presents a clinical trap. It may tempt the clinician to cancel surgery," the case report authors wrote. "However, our systematic review reveals that while some regressions are complete, many are partial or transient. Furthermore, in the biopsy group, nearly 40% of resected specimens still contained residual tumor cells despite clinical regression."

They recommended removing the tissue where the tumor had been regardless of the regression, in case some cancer cells persist. The authors also told New Scientist that they hope to unravel exactly what happens in these rare regressions in order to replicate it through some sort of treatment.

For more intriguing medical cases, check out our Diagnostic Dilemma archives.

This article is for informational purposes only and is not meant to offer medical advice.

A strange divergence is happening in the diagnosis of colorectal cancer: Older people, who are most at risk from the disease, are seeing fewer cases while people under 50 are seeing more.

These diagnoses are often devastating, as younger people also tend to go longer between first experiencing symptoms and getting diagnosed, meaning most of their cancers are caught in a late stage that is more difficult to treat.

"Almost all my patients are my peers, many of whom have young kids or are pregnant themselves or navigating the challenges of just establishing their careers," Dr. Geoffrey Buckle, a gastrointestinal medical oncologist at University of California, San Francisco Health, told Live Science. "They're hit with these obviously extremely scary diagnoses."

But what's driving this rise in young people? Doctors and researchers think some change that occurred after the 1960s is to blame, likely a shift in people's environments or lifestyles. Perhaps offering a clue as to the culprit, recent research also suggests that, whatever the factor, it primarily affects cancers of the rectum and the lowest part of the colon.

The rise of colorectal cancer in young adults

There were about 158,850 new cases of colorectal cancer diagnosed in the U.S. in 2026, according to the American Cancer Society (ACS). Over 86,000 cases — more than half — occurred in people over 65. But those numbers represent a decline of 2.5% a year in that age group since 2013.

Doctors chalk up the decline in colorectal cancer in people 65 and older up to the success of screening, said Dr. Aasma Shaukat, a gastroenterologist at New York University Langone Health. During routine colonoscopies, which start at 45 years old for people at typical risk, doctors remove precancerous polyps and thus prevent that tissue from becoming cancerous.

At the same time over-65s have seen lower cancer rates, people between 50 and 64 have seen a 0.4% increase per year and people between the ages of 20 and 49 have seen an even more alarming jump of 3% each year. The rise is seen in every racial and ethnic group.

What that translates to, according to research published in ACS's CA: A Cancer Journal for Clinicians, are 24,640 new cases a year for people 49 and younger and 47,600 new cases a year for people 50 to 64.

Most of these cases are what doctors call "left-side" cancers, occurring in the lower colon, which descends down the left side of the body, and the rectum. Between 1999 and 2023, rectal cancer mortality rose two to three times faster than colon cancer mortality across all demographics, according to research presented in May at Digestive Disease Week 2026, a major gastroenterology conference.

Possible environmental factors at play

Cancers arise due to genetic errors, some of which occur randomly when cells divide. And the cells in the gut divide constantly: The entire lining of the colon is shed and replaced every week, Shaukat said. The body has mechanisms to repair the myriad DNA mistakes that happen during this turnover, but when the rate of errors increases too quickly or when repair mechanisms fail, that's when most colorectal cancer occurs.

The environment in the gut can affect both this error rate and the efficacy of repair. Researchers have found that there's a complicated feedback loop between the gut microbiome, meaning the community of microorganisms in the colon, and health factors such as diet, exercise and insulin resistance.

Inflammation also factors into this feedback loop. While inflammation is a necessary immune response that repairs damaged tissue with new cell growth, when it becomes chronic, dividing cells become prone to mutation and overproliferation — in other words, cancer.

The culprits for increased chronic inflammation are many, Dr. Theodore Levin, a researcher and clinical lead for colon cancer screening at Kaiser Permanente Northern California, told Live Science. But "these are all thoughts or hypotheses," he cautioned.

One is the rise in sedentary lifestyles and obesity, which contributes to insulin resistance and, in turn, disrupts the microbial colonies that live inside the intestines. These microbes aid digestion and release compounds that can either promote or reduce inflammation.

Childhood antibiotic use rose after the 1960s, which can also perturb the gut microbiome. Additionally, microbiome-disturbing dietary changes since the 1960s include a rise in sugar-sweetened beverages, Levin said, as well as the introduction of a greater number of ultraprocessed foods, which typically lack the fiber content of fresh fruits and vegetables. Fiber, he said, promotes a diverse gut microbiome that tends to tamp down inflammation. (Fermented foods do the same thing, research suggests.)

Researchers are also concerned about the ubiquity of plastics, Levin added.

Some lab research suggests that colorectal cancer cells can take up microplastic particles and that the takeup of those particles increases the cells' propensity to migrate — at least in a lab dish. That could hint that microplastics make cancer more likely to spread through the body. Some animal studies also find that microplastics hamper immune function, which could theoretically help cancer cells to escape the body's defenses.

Plastic particles might also carry carcinogenic compounds deep into the gut, Levin said. Research is still ongoing, but some evidence links chronic exposure to perfluorooctanesulfonic acid (PFOS), a type of "forever chemical" found in nonstick cookware and firefighting foams, to colorectal cancer risk. Experiments using mouse intestinal tissue finds that PFOS reduces a gut enzyme that protects against cancer while spurring the production of proteins that encourage tumor growth.

But researchers have not yet found "one smoking gun" to explain the rise, cautioned Michael Sapienza, the Chief Executive Officer of the nonprofit Colorectal Cancer Alliance. For example, the results of observational studies of forever chemical exposure and colorectal cancer rates are mixed, with some even finding that more PFOS in the blood actually correlates with fewer colorectal cancer cases.

So while the hypotheses are many, the evidence remains murky. Older adults are exposed to all of these environmental and lifestyle changes, too, so researchers also need to understand why their cancer rates aren't rising along with those in younger people. It could be that the removal of precancerous lesions during colonoscopies are masking what would otherwise be a similar rise in the over-65s. Or perhaps it's early childhood exposure that matters most, a risk factor that the oldest adults escaped.

Raising awareness of the symptoms

Scientists aren't entirely sure why cancers of the lower colon and rectum are rising faster than the "right-sided" cancers of the upper intestines.

The lower and upper parts of the colon are very different, Levin said, even arising from different parts of the embryo in the very earliest stage of development. Cancers on the right side and left side often show different genetic mutations. Left-sided colorectal cancer frequently arise from what researchers call chromosomal instability, or mistakes in how chromosomes split between dividing cells during replication, when cells make a copy of their DNA before dividing. Right-sided cancers are more prone to arise from problems with DNA repair during replication.

These differing pathways could help researchers link environmental and lifestyle factors with the changes that lead to colorectal cancer. But that research will take time. For now, gastroenterologists are hoping to raise awareness about the symptoms of the disease and make sure other doctors think to check younger patients for cancer.

Early symptoms include rectal bleeding, unexplained weight loss, anemia, abdominal pain, blood in the stool, changes in bowel habits and unexplained nausea and vomiting. Unfortunately, many early symptoms of colorectal cancer match those of much less serious conditions. For instance, rectal bleeding can be caused by hemorrhoids, and changes in bowel habits could arise from anything from stress to an infection.

Jenna Scott, 40, of Atlanta was 29 and pregnant when her symptoms started. She didn't get a diagnosis until she was 31. By that time, the cancer was metastatic, having spread to other organs. Scott remains in treatment today.

"I don't know if it would have been as aggressive if they had caught it a year-and-a-half earlier," she told Live Science.

Scott's initial symptom was rectal bleeding, but her doctor brushed it off as hemorrhoids caused by pregnancy. Another classic colorectal cancer symptom, weight loss, seemed like typical postpartum shifts on the scale. Health systems and organizations like the Colorectal Cancer Alliance are working to raise awareness among doctors in all specialties so that they check these symptoms out thoroughly in young people rather than explaining them away.

Although routine colon cancer screenings don't start until 45, patients should be pushy with their doctors to get checked out earlier if they have any telltale symptoms, Sapiena said.

"It doesn't mean you have colorectal cancer," Sapiena said of these symptoms. "But it does mean you need to be your own advocate" and seek screening ASAP.

This article is for informational purposes only and is not meant to offer medical advice.

A new artificial intelligence (AI) model can help doctors detect pancreatic cancer up to three years before physicians typically spot tumors on CT scans, a new study suggests.

The program, described April 28 in the journal Gut, was used to analyze almost 2,000 CT scans that had been previously cleared as "normal," bearing no signs of disease. The tool identified tiny irregularities in the structure of the pancreas that later developed into tumor tissue.

Early detection is the single biggest factor in pancreatic cancer patients' survival. Therefore, the model could potentially enable physicians to begin effective treatment while the disease is still curable, the study authors said.

A chance to detect cancer early

Pancreatic cancer is one of the deadliest cancers.

"The five-year survival rate [in the U.S.] is about 12% to 13% because of our inability to detect it at a time when therapeutic options could work their magic," study co-author Dr. Ajit Goenka, a radiologist and nuclear medicine specialist at the Mayo Clinic in Rochester, Minnesota, told Live Science. The early stages of pancreatic cancer often don't trigger any symptoms, so the disease is often advanced at the point of diagnosis.

Although doctors' ability to catch and treat many other cancers has improved in recent decades, no corresponding breakthrough has been seen in pancreatic cancer. Diagnosis typically involves a combination of tissue sampling and imaging tests, including CT scans. But by the time tumors are visible via these methods, the cancer is often terminal.

However, there may be earlier markers of the disease.

"The basic science research tells us that the process of cancer development is not something that starts six months earlier," Goenka said. "It starts 10 to 15 years earlier, which means that there was a signal in the pancreas and that signal was outside the purview of human detectability."

Leveraging AI to recognize patterns that humans cannot, Goenka and colleagues developed a tool to amplify that existing signal and identify early signs of disease in CT scans.

The model, dubbed Radiomics-based Early Detection Model (REDMOD), essentially converts the CT scan image into a mathematical puzzle. It first segments the organ, building a 3D model of the pancreas from the 2D images captured by the CT machine. Then, it evaluates the resulting structure pixel by pixel.

"It's taking each and every pixel in that image and it is quantifying the degree to which it differs from the rest of the organ, and then it's comparing that against the controls where you don't expect that change to be present," Goenka explained. "At the end of the day, it's mathematics. It converts that image into a mathematical representation and extracts those mathematical features."

The team tested the model on a sample of 2,000 existing CT scans, which were previously collected for medical issues unrelated to cancer and had all been signed off as normal. About one-seventh of the scans belonged to patients who later went on to develop pancreatic cancer.

The model successfully identified 73% of these early-stage cases, and on average, the scans the model analyzed had been taken 16 months before the person's actual diagnosis.

"The sensitivity gain over radiologists was nearly twofold across the spectrum, and when you look at even earlier — more than two years prior to diagnosis — that sensitivity gain was almost threefold," Goenka said. In other words, the AI tool correctly identified cancer cases earlier than radiologists did, and the earlier in time you look, the greater that performance gap grew.

Next steps

That said, the AI tool has room for improvement. "The radiologist was less likely to flag a healthy patient incorrectly," Goenka noted. The model correctly identified disease-free patients 81.1% of the time, compared with an average of 92.2% for human radiologists. "So there is a complementary role for both of them, for physician expertise combined with AI augmentation."

The study was very well designed and produced some extremely promising results, said Tatjana Crnogorac-Jurcevic, a professor of molecular pathology and biomarkers at Queen Mary University of London who was not involved in the work.

"Such early detection would make a huge change in the clinical workup of the patients," she told Live Science. "Because pancreatic cancer is fairly uncommon, general screening as we have now for colon and breast is not going to be feasible, but there are defined high-risk groups for which surveillance will be possible — individuals with a family history of pancreatic cancer, those with other cancer mutations, and patients with new-onset diabetes."

Goenka hopes the model could be routinely implemented in the clinic within the next five years, and the team is currently running clinical trials to further validate that this detection strategy works in practice.

Looking forward, combining this REDMOD with other diagnostic methods could yield even greater gains in early detection, Crnogorac-Jurcevic said.

"We are developing urine-based tests with exactly the same aim, and having an AI imaging tool to combine with our body fluid biomarkers would be fantastic," she said. "It's highly likely that they will be complementary, which would increase the sensitivity and accuracy of early detection massively."

This article is for informational purposes only and is not meant to offer medical advice.

The force of a pumping heart changes how cancer cells function, halting their ability to multiply and spread, a new study shows.

The finding may help to explain why heart cancer is so rare, occurring in fewer than 2 in 100,000 people per year.

A protein called Nesprin-2 is key to this phenomenon. Found in the outer membrane of a cell's nucleus, the protein was already known to sense and respond to mechanical forces. Now, Nesprin-2 has been found to sense the force of heartbeats and stop cancerous cells from multiplying.

In addition to offering a possible explanation for why heart cancer is so rare, the findings could open the door for new therapies for other cancers, researchers concluded in the study, which was published April 23 in the journal Science.

We're going to "try to exploit this knowledge to develop a mechanical therapy for cancer," study author Serena Zacchigna, head of the Cardiovascular Biology Laboratory at the International Centre for Genetic Engineering and Biotechnology in Italy, told Live Science.

Zacchigna and colleagues are developing bands that can be strapped around tumors on the skin and then reproduce the force of a beating heart. Because metastatic skin cancer is one of the more common cancers to spread to the heart, this is a good first clinical case to look at, Zacchigna said.

Heartbeats subdue cancer

Both primary heart cancer, which starts in the heart, and secondary heart cancer, which spreads to the organ from other places, are fairly rare. The reason for this rarity is a long-standing mystery.

The mechanical load of heartbeats, meaning the physical force they exert, has been found to limit the ability of heart tissue to regenerate. So Zacchigna and her colleagues wanted to see if heartbeats might also stop cancerous cells from multiplying.

First, they implanted lung cancer cells into the hearts of lab mice to observe the cells' growth and spread. The hearts were either beating normally or were "unloaded," meaning they were attached to a blood supply but not actively pumping. Beating hearts seemed to stave off cancer growth, while the unloaded hearts saw a massive proliferation of cancerous cells.

The team ran a similar test with rat heart tissue grown in lab dishes. They found that tinkering with the amount of mechanical load in the tissue affected the behavior of lung cancer cells; the cancer grew and spread more when the mechanical load was reduced.

To understand what causes this phenomenon, the team took tissue samples from human patients whose lung, colon or skin cancer had spread to the heart and other organs. They mapped the gene activity of those cancer cells and zoomed in on their epigenetics, the markings "on top of" DNA that control which genes are switched on.

They found that certain epigenetic markers were tied to tumor growth and confirmed that heartbeats reduce these tumor-related markers. From there, they identified Nesprin-2 as a key player — switching off Nesprin-2 in "beating" heart tissue increased cancer proliferation.

These findings are the first to show that mechanical forces beyond the tumor itself affect the growth and spread of cancerous cells, Zacchigna said. The ability for mechanical forces to thwart cancer proliferation also appears to be a general mechanism, as "we saw that this signature is common to many cancer types," she said.

Possible treatments?

These findings are "of consequential importance," said Julie Phillippi, a chair of cardiothoracic surgery and head of the Cardiac Research Laboratory at the University of Pittsburgh, who was not involved in the research.

In an email, she told Live Science that the findings could also shed light on how to regenerate heart tissue in a targeted manner. And because heart cancer is so rare, "this work may have stronger impact in the context of cancers in other organs," she added.

The potential of using mechanical stimulation in cancer therapies is an "exciting idea to pursue," Phillippi said. But it requires a better understanding of how the properties of the tissue surrounding cancer cells affect their ability to sense mechanical forces.

With their new cancer-shaking bands, the team hopes to start a clinical trial within four years. For that, they'll need the first prototypes of these systems ready for human use, Zacchigna said. It will be key to identify the right time to implement the therapy and the patients who would benefit most, she noted.

A major challenge is to confirm this mechanical stimulation is a safe procedure, Zacchigna said.

"My fear is that by squeezing a tumor we may favor its dissemination," she said. "This is something we really have to rule out before moving forward."

Another approach could be to find drugs that can mimic the epigenetic effects of heartbeats, without the need for mechanical stimulation. The team is exploring that idea, too.

This article is for informational purposes only and is not meant to offer medical advice.

Colorectal cancer — cancer of the large intestine or rectum — is now the leading cause of cancer deaths in people under 50 in the U.S., a new study finds.

Colorectal cancer incidence and mortality have been increasing in people under 50 each year since 2013 and 2004, respectively, according to research published March 2 by the American Cancer Society (ACS). This rise in early onset diagnoses is driven by advanced-stage disease. (Colorectal cancer is also known as bowel cancer.)

"The trend is very serious," study co-authors Rebecca Siegel, Nikita Sandeep Wagle and Dr. Ahmedin Jemal told Live Science in a jointly written email. Siegel is senior scientific director of cancer surveillance research at the ACS; Sandeep Wagle is principal scientist of cancer surveillance research at the ACS; and Jemal is senior vice president of surveillance, prevention and health services research at the ACS. "Colorectal cancer is the only common cancer [in people] under 50 with rising mortality," they wrote.

Incidence is also increasing among adults aged 50 to 64, with the disease being diagnosed at more advanced stages. This is thought to be linked to the similarly increased mortality in this age group, the authors wrote in the study.

The trend in people under 65 is in marked contrast to the decreasing rate of new bowel cancer cases and deaths in adults ages 65 and over. Because most cases are in people 65 and over, this declining trend is masking an opposing pattern among the younger cohorts, the authors wrote in the study.

A troubling trend

Colorectal cancer is the second-leading cause of cancer deaths globally and mainly affects people 65 and over. But colorectal cancer "can no longer be called an old person's disease," Jemal said in a statement. Indeed, a 2025 analysis revealed that colorectal cancer cases were simultaneously rising in people under 50 and either stabilizing or declining in 50- to 74-year-olds in 14 countries, including the U.S., Canada, Australia and England.

But in the new study, the researchers compiled data on the number of new colorectal cancer cases from 1998 to 2022 alongside the number of colorectal cancer deaths from 1930 to 2023, while zooming in on slightly different age cohorts. The data were drawn from the National Cancer Institute and the Centers for Disease Control and Prevention (CDC).

By narrowing the age ranges examined, the team found that the rise is occurring not just in people under 50 but also in people up to 65 years old. "The increase in colorectal cancer is not just in young people, per se," the study authors told Live Science.

This phenomenon is called the "birth cohort effect," meaning that when an individual was born is more closely related to disease risk than when they were diagnosed. This confirms "a real uptick in disease because of something we're doing or some other exposure," Siegel said in a statement.

However, it remains unclear what is causing this trend, the authors wrote in the study.

"Long-established risk factors for colorectal cancer were identified based on cancer in older adults who were exposed to different risk factors than those in more recent generations," Siegel, Sandeep Wagle and Jemal told Live Science. For example, for all ages combined, almost 14% of colorectal cancer is attributable to smoking, but people under 50 are less likely than older adults to have smoked, they said.

Since the second half of the 20th century, individuals have been exposed to new environmental factors that may raise cancer risk, such as microplastics and ultraprocessed foods, they said. Research has also previously found colorectal cancer is associated with high antibiotic exposure and processed meat.

Colorectal cancer screening saves lives

The team estimated there will be 158,850 new cases of bowel cancer in 2026. Of those, 47,600 will be in 50- to 64-year-olds and 24,640 will be in those under 50. Over 55,000 people of all ages are projected to die from the disease this year. Of those, 7% will be in those under 50 and 24% will be in people aged 50 to 64.

With most people under 50 being diagnosed with an advanced stage of the disease, which is harder to treat, earlier diagnosis is essential, Siegel, Sandeep Wagle and Jemal told Live Science.

"Earlier diagnosis can also be achieved by increasing awareness of symptoms for colorectal cancer like blood in stool, abdominal pain, diarrhea, or fatigue, which can often be mistaken for other health issues," they said. "Earlier attention to symptoms could help shift diagnoses toward earlier, more treatable cancer"

Screening also allows for earlier detection and removal of precancerous lesions in the bowel; which accounts for 79% of averted colorectal cancer deaths. Current ACS guidelines state average risk individuals — those without a personal or family history of the disease — should begin colorectal cancer screening from age 45. Medicare covers various screening tests from this age, including a stool DNA test and colonoscopy. There are no specific ACS guidelines for high risk individuals, but they may require earlier and more frequent screening.

However, the researchers found that only 37% of 45- to 49-year-olds are up-to-date with their colorectal cancer screening. With half of deaths in people under 50 being in 45- to 49-year-olds, this means that many colorectal cancer deaths in this cohort could be prevented, Siegel, Sandeep Wagle and Jemal said.

This article is for informational purposes only and is not meant to offer medical advice.

A vaccine designed to fight HPV-driven head and neck cancers has shown promising results in a lab study in human tissues and mice.

If proven effective in humans, the therapeutic shot could complement standard cancer therapies, and its design may help scientists build better vaccines for other diseases.

Human papillomavirus (HPV), the virus behind most cases of cervical cancer, also causes several other cancers, including oropharyngeal cancer (throat cancer). In the U.S., about 70% of oropharyngeal cancers are linked to HPV. While over 100 strains of HPV exist, only 12 types are considered "high-risk" for causing cancer; almost all cases of HPV-related throat cancer are caused by the high-risk HPV strain 16.

The vaccine Gardasil 9 can prevent HPV infections and thus reduce the risk of these cancers down the line. But for people who already have HPV-related tumors, treatment still relies on surgery, radiation and chemotherapy. Combining a cancer vaccine with these conventional therapies could enhance their effectiveness by teaching the immune system to fight the cancer.

Now, scientists have engineered a cancer vaccine whose components are arranged in a unique structure. Similar to preventive vaccines, cancer vaccines train the immune system to recognize specific proteins — in this case, a protein found on HPV-positive tumors — and often contain ingredients called adjuvants that rev up the immune response. Rather than preventing the disease in the first place, though, cancer vaccines are generally used to treat the disease and help prevent its recurrence.

In lab studies of HPV-positive head and neck cancer, this new, carefully crafted vaccine slowed tumor growth and improved survival in mice, according to a study published Wednesday (Feb. 11) in the journal Science Advances.

Dr. Ezra Cohen, a head and neck cancer specialist at UC San Diego Health who was not involved in the study, said that if the vaccine works in humans, it could complement standard therapies.

"One can imagine a multi-modality approach to render a patient disease-free and then the vaccine to prevent recurrence," he said. But he cautioned that results in lab animals and isolated tissues don't always translate to humans. "The real test is in people," he told Live Science in an email. "But strong preclinical data, like these, make the chances of success in clinical trials higher."

In this case, the vaccine's underlying design is notable.

"The key finding is that the structure of the vaccine makes a significant difference," Cohen said. "Successful vaccination is not just about selecting the correct antigens [target proteins] but placing those antigens in the right sequence with other vaccine elements."

The vaccine uses spherical nucleic acids (SNAs) — globe-shaped DNA particles that enter immune cells and bind to targets more effectively than linear DNA does. Each SNA nanoparticle within the vaccine consists of a fatty core surrounded by an adjuvant and a fragment of an HPV protein from the tumor cells. The adjuvant mimics bacterial DNA and is recognized by the immune system as "foreign."

The researchers tested three designs, changing only how the HPV fragment was positioned. One version hid it inside the nanoparticle, while the other two versions had the HPV fragment on the surface of the particle, attached at different ends of the fragment's structure, known as the N terminus and the C terminus.

The version with the fragment attached to the surface via its N terminus triggered the strongest immune response, the team found. This design led killer T cells — immune cells that destroy infected, damaged and cancerous cells — to produce up to eight times more interferon-gamma, a key antitumor signaling protein. This made them more effective at killing HPV-positive cancer cells.

In mouse models of HPV-positive cancer, the vaccine significantly slowed tumor growth. Additionally, when tested in tumor samples collected from HPV-positive cancer patients, the N-terminus vaccine killed two to three times more cancer cells compared with the other two vaccine designs.

"This effect did not come from adding new ingredients or increasing the dose. ​It came from presenting the same components in a smarter way," study co-author Dr. Jochen Lorch, the medical oncology director of the Northwestern Medicine Head and Neck Cancer Program, said in a statement.​

"The immune system is sensitive to the geometry of molecules," he said. "​By optimizing how we attach the antigen to the SNA, the immune cells processed it more efficiently."

Looking ahead, study co-author Chad Mirkin, inventor of SNAs and director of Northwestern's International Institute for Nanotechnology, hopes this approach could help scientists redesign older vaccines that initially seemed promising but failed.

"This approach is poised to change the way we formulate vaccines," Mirkin said in the statement. "We may have passed up perfectly acceptable vaccine components simply because they were in the wrong configurations. We can go back to those and restructure and transform them into potent medicines."

This article is for informational purposes only and is not meant to offer medical advice.

A first-of-its-kind trial demonstrates that AI-assisted mammography can improve the outcomes of patients with breast cancer, particularly those with aggressive disease.

While many people have only recently begun to use artificial intelligence (AI) in their everyday lives, the technology's use in medicine began about a decade ago, especially in the field of image-based diagnostics. Researchers have been training AI programs to recognize tumors and other signs of disease in various medical imagery, such as X-rays, MRIs, and tissue biopsies mounted on slides.

These images have been taken primarily from patients whose diagnoses were already known, in "retrospective" studies. Knowing the diagnosis enabled doctors to provide feedback to the AI, confirming that it correctly identified cancer or determined an image was cancer-free. These studies have shown that AI could be an invaluable tool in diagnostic medicine.

However, to know if an AI tool can really diagnose cancer and make a difference to patients, you need to have a "prospective" study — one in which patients who are diagnosed using the AI tool are then followed for several years to determine their health outcomes.

Now, researchers in Sweden have conducted a gold-standard trial to assess the use of AI in mammography screening. Results from the Mammography Screening with Artificial Intelligence (MASAI) trial, published Jan. 31 in the journal The Lancet, showed that mammography reading supported by AI can improve screening performance while reducing radiologists' workload.

This is the first time AI has been shown to improve the outcomes of patients with breast cancer.

Spotting cancer earlier

The practice of regularly screening patients has significantly reduced the incidence of late-stage cancer and breast cancer deaths in much of the world. But even with regular mammograms, some cancer may go undetected.

These "interval cancers" are not detected at an initial screening but get diagnosed within the next two years, or between two screening rounds. They are often missed because they are masked during the initial screen due to breast-tissue density or the tumor disguising itself as normal tissue. Or sometimes, they can develop very quickly between screening dates.

These cancers are invasive, spreading into nearby healthy tissues, and typically aggressive, resulting in worse patient outcomes. Declines in interval cancer rates are the best way to confirm that a screening method works, meaning it drives down late-stage cancer diagnoses by spotting more cases earlier.

"If you want to improve the efficacy of screening, then the interval cancer rate is a very good surrogate measure of breast cancer mortality," senior study author Dr. Kristina Lång, a breast radiologist and clinical researcher at Lund University in Sweden, told Live Science. "So if we can lower the interval cancers, it will likely have a positive impact on patient outcomes."

The MASAI trial included more than 100,000 women between the ages of 40 and 80 living in Sweden. It used a commercially available AI system that was trained on more than 200,000 examinations from medical institutions all over the world.

In a comparison group, mammograms were read by two radiologists, as is the standard in Sweden. In the AI-assisted group, the AI system analyzed mammograms for suspicious findings and provided a risk score of 1 to 10. Cases with a score of 1 to 9 were subsequently read by a single radiologist, while a score of 10 would be read by two radiologists. The AI system was also able to highlight the suspicious findings within the image so the human radiologists could easily review them.

The AI-supported screening identified more clinically relevant cancers than unassisted mammography did. "Clinically relevant" cancers are those that have the potential to progress and thus require medical intervention.

It also reduced the number of interval cancer diagnoses within the two years following the screen. This shows that the AI program was more effective at identifying cancers that might normally be missed by a human radiologist, allowing medical treatments to start earlier.

Reducing false positives

While cancer screening is mostly beneficial, there are some potential downsides, such as false positives and overdiagnosis. When a patient is called back for a recheck after a screening but does not have cancer, "that can be a really stressful experience," Lång said.

The latter situation, overdiagnosis, refers to situations where a screen detects a cancer that will ultimately cause no harm to the patient. Such cancers grow so slowly that they won't cause symptoms within a patient's lifetime or increase the chance of death. Overdiagnosis can subject healthy patients to unnecessary cancer treatments.

The goal of AI-assisted mammography is to improve the ability of the screening test to find cancer while mitigating these potential negative effects — and the study found that AI-assisted screening did not increase the risk of false positives and that it improved the detection of clinically relevant cancers.

Along with improving cancer detection, AI-assisted screenings could address the consistent shortage of radiologists available to provide cancer screening.

"In some places, you're lucky to find one radiologist to read the mammograms," said Dr. Richard Wahl, a radiation oncologist at Washington University in St. Louis who was not involved in the study. "If you don't have the expert radiologists, women can't benefit like they should from screening programs."

Additionally, as the few radiologists available work more hours, their performance decreases. But AI doesn't get tired, and its performance doesn't decline at the end of the workday.

"The workforce issue is real, and this [study] could have an impact," Wahl said. "I think people will gradually be interested in having AI-aided interpretation as a second set of eyes."

Lång and her team will be starting a screening trial in Ethiopia in March, during which they will use AI to support the rapid assessment of breast cancer using bedside ultrasounds within a screening program.

"The problem in these settings where they don't have a screening program is that many women come in with late-stage disease, and there are no radiologists there," Lång said. With AI support, Lång hopes to improve access to accurate screening and thus enable earlier diagnosis of breast cancer in these limited resource settings.

This article is for informational purposes only and is not meant to offer medical advice.

Around 90% of people are infected with Epstein-Barr virus at some point in their lifetimes. For most of them, the virus causes a mild, transient illness or no symptoms at all. But for a subset of people, Epstein-Barr can eventually contribute to chronic illnesses, such as lupus and multiple sclerosis, or to the development of cancer.

Now, new research uncovers 22 human genes that might make an Epstein-Barr infection more likely to turn into a chronic condition.

Researchers can't yet definitively say whether these genes directly make Epstein-Barr more dangerous, or whether they are part of an underlying immune suppression that allows the virus to persist at higher levels in the body than usual. But the new study should provide a jumping-off point, said Jill Hollenbach, a professor of neurology at the University of California, San Francisco, who was not involved in the study.

"My lab is already looking into the results and thinking about what we can learn from this and what other avenues of research it suggests," Hollenbach told Live Science. Hollenbach wrote a commentary of the new study accompanying its Jan. 18 publication in the journal Nature.

Nearly two dozen genes

Epstein-Barr virus can cause mononucleosis, better known as mono, a temporary illness notable for producing extreme fatigue. But even once the symptoms of mono disappear, the virus lies latent in the body, mostly in the immune system's B cells, which remember and defend against specific germs.

For most people, this latent Epstein-Barr virus causes no problems. But in other people, the virus persists at a higher, more active level. In these cases, it can raise the risk of certain nasopharyngeal cancers and lymphomas, and may fuel autoimmune disorders such as multiple sclerosis. Chronic, active Epstein-Barr has also been linked to heart and lung disease.

To understand why only some people seem to experience these chronic effects, Ryan Dhindsa at the Baylor College of Medicine and colleagues turned to an underexplored source of information: human DNA biobanks. These biobanks collect full gene sequencing data and health records for hundreds of thousands of individuals. In sequencing the human genome, they also happen to scoop up the DNA of any viruses that happen to be in residence inside cells.

"Typically, when we're analyzing human genome sequence data we ignore the reads that don't map back to a human reference genome. We just kind of throw them away," Dhindsa told Live Science. "Here, we decided maybe we could go through those reads that we normally throw away and see if we could recover viral DNA."

By combing through tossed-aside Epstein-Barr sequences from 750,000 people in the UK Biobank and the U.S. National Institutes of Health's All of Us biobank, the researchers were able to identify individuals — about 11% of the total — who had very high levels of Epstein-Barr DNA. They found that these high levels of viral DNA were associated with health conditions previously linked to Epstein-Barr, including diseases of the spleen and Hodgkin lymphoma.

The presence of viral DNA was also associated with conditions thought to be linked to Epstein-Barr, although less definitively: rheumatoid arthritis, chronic obstructive pulmonary disease (COPD), and lupus. Other associations in the data reinforce even less well-studied connections, including links between Epstein Barr and heart disease, kidney failure, stroke and depressive episodes.

In addition, the researchers found 22 genes tied to a higher likelihood that someone would be in the 11% of people with chronic Epstein-Barr. Many of these genes were in a region of the genome called the human leukocyte antigen (HLA) locus, which is known to code for the immune cells that present antigens — immune-response-triggering foreign molecules — to other immune cells.

"It seems like these variants changed the way an individual's immune response actually presents Epstein-Barr virus to the immune system," Dhindsa said, possibly making it harder for the body to suppress viral replication. That said, the data has only shown a link between these genes and persistent infection — more research is needed to prove cause-and-effect.

In people with high levels of Epstein-Barr, the researchers also saw variations in genes that regulate the immune system. One, the SLAMF7 gene, typically encodes for a cell-surface protein that helps the immune system's natural killer cells attack tumors. Another, called CTLA4, encodes for a receptor on T cells that helps keep the immune system from attacking the body.

"They found some really interesting results," Hollenbach said.

She and her team are now interested in looking deeper at the mechanisms that link the genetic variation to the immune response to Epstein-Barr. Meanwhile, Dhindsa and his colleagues are interested in using biobank data to search for other viruses that have long-term impacts on human health. Some examples are the cancer-causing viruses Merkel cell polyomavirus and human T-cell lymphotropic virus type 1.

The researchers are also eager to expand their methods to more diverse global datasets of human genes. While the All of Us dataset includes participants from a variety of backgrounds, the U.K. Biobank is predominantly made up of people of European ancestry.

"We need to be able to look at genetic differences across more representative samples in future work," he said.

A triple-drug therapy for pancreatic cancer has shown promise in early animal tests, pointing to a potential new treatment for a disease with a notoriously low survival rate.

Considered one of the deadliest common cancers, pancreatic cancer has a five-year relative survival rate around 13% — meaning roughly 87% of people with the cancer are expected to die within five years of diagnosis. That survival rate can plummet as low as 1% for people diagnosed in very late stages of the disease.

Now, in a study published Dec. 2 in PNAS, researchers tested a new combination therapy that blocks three cancer-growth pathways simultaneously and shows promising results in mice.

"These studies open a path to designing new combination therapies that can improve survival for patients with pancreatic ductal adenocarcinoma [the most common pancreatic cancer]," the study authors said in a statement. "These results point the way for developing new clinical trials."

Early-stage pancreatic cancer grows silently inside the abdomen without any obvious symptoms. By the time the disease is detected, it has often already spread to other organs, making it difficult to remove surgically.

Standard treatments like chemotherapies attack all rapidly dividing cells in the body, often causing a lot of collateral damage in the process of controlling tumor growth. And even then, tumors usually find alternative ways to multiply and become resistant to treatment.

The new therapy not only prevented the rodents' cancer from coming back, but it was also non-toxic for mice overall, showing no debilitating side effects.

Nearly all pancreatic cancers are associated with a mutation in a gene called "KRAS," which normally controls cell division and growth, keeping it in check. But when the gene is mutated, it gets stuck in an "on" position, leading to abnormal rate of cell division and cancer.

Prior to the current research, senior study author Carmen Guerra, a cancer biologist at the Experimental Oncology Group of the Spanish National Cancer Research Centre (CNIO), developed mouse models to investigate how KRAS mutations and other related pathways help pancreatic tumors survive. While blocking certain KRAS-related pathways can stop small tumors from growing, larger tumors often adapt to "open another door" for survival, she told Live Science.

In their latest work, Guerra and her team analyzed these resistant tumors, discovering that a protein called STAT3 became highly active when other growth routes were blocked. That suggested that it might be acting as the emergency backup pathway for tumor growth.

The team tried genetically blocking this pathway in mouse tumor cells, along with other major tumor-growth drivers. And they observed that the tumors regressed, confirming that STAT3 was indeed a key "mechanism of resistance," Guerra said.

At that point, the researchers had confirmed that genetically shutting down three pathways — KRAS, a KRAS-related pathway, and STAT3 — could eliminate tumors. So they set about testing a drug-based version of the strategy.

This triple-pronged approach includes two existing drugs: afatinib, which is approved by the Food and Drug Administration for certain lung cancers, and daraxonrasib, which is currently being tested in clinical trials. The third drug is a newer compound designed to disable STAT3.

The team evaluated this three-drug therapy in three types of mouse models: one in which tumor cells from mice are implanted directly into the mouse pancreas; one involving mice that were genetically engineered to develop pancreatic cancer; and one using human tumor samples grown in immune-deficient mice, to prevent mouse immune system from attacking foreign tissue. In all three models, the combination treatment eliminated the tumors completely.

"You couldn't even see where the tumor was," Guerra told Live Science. "The pancreas was completely healthy."

The treatment also prevented resistance, as the team reported that the tumors did not return for at least 200 days — or nearly seven months — after the treatment, which is longer than what most single-drug therapies achieve in similar mouse models.

Importantly, the triple-drug therapy did not cause toxic or severe side effects in mice. The rodents receiving the therapy showed similar body weight, blood counts, metabolic markers and organ health when compared to tumor-bearing mice given a placebo treatment.

However, given this new research was in mice, there could be some differences in human pancreatic cancer patients. Guerra noted that mice can be "more resistant to this kind of toxicity" than humans are. While the therapy didn't show any side effects in mice, some drugs they used, like afatinib, have already been tested in humans and are known to have some side effects, such as skin and gastrointestinal issues.

So, the researchers are now working to find alternatives and "develop better drugs" that hit the same pathways, she told Live Science.

Guerra also stressed that pancreatic tumors are genetically diverse, and patients can have "tons of alterations," making each case different to the next. On that front, the team will also study additional mouse models that carry other common KRAS mutations, as well as changes in other cancer-related genes, to test the effectiveness of the therapy in a diverse range of tumors, she told Live Science.

This article is for informational purposes only and is not meant to offer medical advice.

Could being colorblind make you less likely to survive bladder cancer? That's the surprising hypothesis that researchers have proposed based on a small study.

The research, published Jan. 15 in the journal Nature Health, examined data from 135 patients with both bladder cancer and color blindness, and compared those patients to 135 patients with only bladder cancer. The data were taken from TriNetX, an international registry of electronic health records of more than 275 million patients.

Among these health records, people who had both color blindness and a bladder cancer diagnosis had shorter survival times than did bladder cancer patients without the vision deficiency. Overall, those with color blindness had a 52% higher risk of dying within 20 years of their bladder cancer diagnosis, compared with the normal-vision group.

The study authors suggested a plausible reason for this observed difference: Color blindness may make it more difficult to spot blood in your urine — an early sign of the cancer — thereby delaying diagnosis.

"Bladder cancer is a bad disease. If you delay your diagnosis, it will make a difference to your prognosis," Dr. Veeru Kasivisvanathan, a urological oncologist and surgeon at University College London who was not involved in the study, told Live Science.

A possible link

Blood in urine is one of the most common early symptoms of bladder cancer, alongside frequent urination; pain or burning during urination; feeling as if you need to urinate even if your bladder isn't full; and urinating frequently during the night.

If anyone spots blood in their urine, they should see their doctor straight away, Kasivisvanathan said. But, as the study authors suggested, being unable to clearly distinguish red from yellow could make it very difficult to spot this early warning sign.

Color blindness, also known as color vision deficiency, is a fairly common condition with one recent study reporting that about 1 in 40 people globally have some form of color vision deficiency. (Those figures are likely approximate, as screening for color vision deficiency is often not routine.) Color vision deficiency tends to be more common in males than in females, per the study.

The results of the new study should be taken with extreme caution, Kasivisvanathan and Shang-ming Zhou, a professor in e-health at the University of Plymouth who wasn't involved in the work, told Live Science. Indeed, the study authors also acknowledged that there are major limitations to their research.

For instance, because color blindness often goes undiagnosed, it's possible that some people with the condition were mistakenly added to the cohort without color blindness in the analysis, potentially muddying the results. The term "color blindness" also encompasses various conditions with different red-perception abilities. Protanopia (red-blindness) should theoretically carry a higher risk than deuteranopia (green-blindness) in this context, but the study cannot differentiate between these subtypes, said Zhou.

In addition, the study was very small, which makes the results less dependable, and makes it difficult to screen for other factors that could explain the difference in prognosis. Lastly, from these data alone, it's not possible to prove that color blindness delayed the diagnosis of the disease; for now, that is just a hypothesis.

"The authors properly frame this as the hypothesis-generating work," Zhou said. "Current evidence is insufficient to recommend routine blood cancer screening in [patients with color vision deficiency], and the absolute risk increase remains unclear," he emphasized.

In short, more research is needed to confirm that color blindness raises the risk of death from bladder cancer, and to evaluate how those patients might be better protected, if that's the case. Still, this is "the right type of [study] design for that type of question," Kasivisvanathan said, adding that while the research is not conclusive, it does open up interesting areas for investigation.

It could be that patients with known risk factors for bladder cancer — such as being a male over the age of 50, smoking, using blood thinners, or having a history of radiotherapy — might benefit from being warned about the potential risk of having undiagnosed color blindness on top of their other risk factors. And perhaps those with known color blindness and cancer risk factors could be encouraged to screen their urine in other ways, such as using test strips, Kasivisvanathan said.

This study also raises questions about other cancers that are associated with blood in bodily fluids in their early stages, such as oral cancers, Zhou added. But for now, more research is needed, all of the experts said.

This article is for informational purposes only and is not meant to offer medical advice.

The 5,300-year-old Ötzi the Iceman mummy and a prehistoric man who lived in Siberia 45,000 years ago both carried a cancer-causing strain of human papillomavirus (HPV), new research finds.

Scientists analyzed ancient genetic data previously collected from the individuals, and found that both were likely infected with HPV16, a preprint paper posted to bioRxiv on Dec. 16, reported. In the study, which has yet to undergo peer-review, the authors present what they say is the "earliest molecular evidence" of HPV16 in modern humans.

This extremely early evidence of HPV16 in modern humans challenges the idea that Neanderthals, who overlapped with us in Eurasia from around 60,000 to 34,000 years ago in Eurasia, were the ones who transmitted the virus to us, the researchers said. But the team acknowledged that their sample size of two is small, so it's still hard to know where HPV16 originated.

HPV in ancient humans

HPV encompasses a diverse family of viruses that are primarily transmitted through direct skin-to-skin or sexual contact, and they are commonly found in humans today. Most infections are symptomless but in a small fraction of cases, HPV16 and other high-risk types (known as "oncogenic" papillomaviruses) can fuel the development of some cancers.

While the clinical significance of papillomaviruses is well understood, little is known about their occurrence among prehistoric human populations. In the study, the authors explored a long-standing question of how far back cancer-linked papillomaviruses — particularly HPV16 — have circulated in modern humans, study co-author Marcelo Briones, a professor at the Center for Medical Bioinformatics at the Medical School of the Federal University of São Paulo, Brazil, told Live Science in an email.

"The results indicate that HPV16 has been associated with anatomically modern humans for a very long time, likely well before major population splits outside Africa," or before 50,000 to 60,000 years ago, Briones said. "This supports the idea that oncogenic human papillomaviruses are not recent pathogens but long-term companions of their hosts, evolving alongside primates and humans over extended evolutionary timescales."

The researchers re-analyzed publicly available genome sequencing datasets for both Ötzi and the Siberian man, known as Ust'-Ishim. These individuals were chosen because they represent two of the best-preserved and best-characterized ancient human genomes available, Briones said.

Ötzi is a naturally mummified man whose 5,300-year-old remains were discovered in 1991 high in the Alps mountain range on the Austria-Italy border. His remarkably well-preserved body, clothing and tools have since provided a rare glimpse into prehistoric life in the region. The Ust'-Ishim man, meanwhile, who was discovered in 2008, lived around 45,000 years ago in what is now western Siberia. His remains — a single leg bone — yielded one of the oldest modern human genomes ever to be fully sequenced.

Briones and colleagues searched the genetic datasets for DNA fragments matching known HPV genomes. They found multiple DNA fragments matching HPV16 (specifically, a lineage known as HPV16A) in both individuals, suggesting the virus was present in them.

Most previous hypotheses about when HPV16 emerged in modern humans relied on computer models of how the virus evolves over time. These suggest the virus has ancient evolutionary origins but lacked direct biological confirmation, according to the researcher. In general, computer models suggest that papillomaviruses likely co-evolved with vertebrates for hundreds of millions of years.

While the preprint does not address the ultimate origins of HPVs as a group, it does show at least one high-risk type was present in modern humans at least 45,000 years ago.

Given this early date, the new findings challenge a previously proposed hypothesis that Neanderthals transmitted HPV16A to prehistoric Homo sapiens populations through interbreeding, Briones said. Although he said the new study's conclusions are "limited" by the small dataset.

Koenraad Van Doorslaer, interim co-chair of the immunobiology department at the University of Arizona who was not involved in the study, told Live Science in an email he "largely" agreed with the paper's conclusions, noting the authors "rigorously demonstrated" that both individuals were likely infected with HPV16.

"I am genuinely excited about the implications of this study because it supports some critical assumptions about the history of this family of important viruses," Van Doorslaer said.

However, Van Doorslaer said the proposal of the study authors that their findings present a challenge to the idea that HPV16A first entered our species due to Neanderthal interbreeding "may be overstated" in light of the data presented. In part, because Ust'-Ishim was previously shown to have Neanderthal DNA in his genome, "suggesting that the interbreeding pre-dates Ust'-Ishim's life," Van Doorslaer said. "So since this sample both has Neanderthal DNA and HPV16 DNA, it does not prove that HPV16 does not come from Neanderthals."

Ötzi quiz: What do you know about the Iceman mummy who was murdered 5,300 years ago in the Alps?

What if a single blood test could determine whether you had one of 14 types of cancer?

That's the question posed by a study published in November in the journal Cancer. Conducted by researchers at the cancer detection-test company Exact Sciences, the paper models how cancer care for five million U.S. adults might be changed by easy access to blood tests designed to spot many cancers — known as multicancer early detection (MCED) liquid biopsy tests.

The study suggests the tests could save lives by catching cancer at earlier stages, when it's more easily treated. It predicted that, over a decade of use, MCEDs could reduce stage IV cancer diagnoses in the U.S. by 45%, compared to the current standard-of-care.

But for now, liquid biopsies that test for multiple cancers still have unacceptably high false-positive rates. And even when they don't, there aren't clear guidelines for how to integrate them into the standard-of-care. That means they aren't going to make their way into the clinic in the near term, experts told Live Science.

Before the transformative effect predicted by the Cancer paper can be borne out, doctors will need to figure out how to best use these tests in the clinic.

The pitch for liquid biopsy

The idea behind liquid biopsy tests is that they enable clinicians to look for cancer without going anywhere near the tumor itself, Dr. Carolina Reduzzi, an oncologist and director of the liquid-biopsy platform at Weill Cornell Medicine, told Live Science.

"It's like translating a tissue biopsy into the blood," said Reduzzi, who was not involved in the Cancer report. These tests can detect various signs of cancer, including individual circulating tumor cells (CTCs), chunks of tumor genetic material floating in the bloodstream, and even tiny fragments of tumor cells.

Because they do not direct tumor sampling, liquid biopsy tests are comparatively simpler and less invasive. Additionally, the hope is that if clinicians regularly repeat liquid biopsies, they could build up a picture of how a tumor changes in response to treatment.

If a patient's tumors contain many genetically distinct cells, tissue biopsies that only sample one portion of the tissue may provide a biased view of their disease, said Reduzzi. Liquid biopsy, in contrast, should provide a broader picture of a patient's cancer by making it easier to analyze cells from multiple tumor sites.

Which tests are in use now?

To date, the U.S. Food and Drug Administration (FDA) has approved five liquid biopsy diagnostic tests, each for single types of cancer. These tests have been validated via assays that compared their ability to detect signs of cancer against tests that sample tumor tissue.

No MCED tests are currently approved or available through routine clinical care, although some, like Exact's Cancerguard and GRAIL's Galleri, are available in the United States as "laboratory-developed tests" (LDTs). LDTs exist in a regulatory gray area in which they are not formally approved by the FDA but are available to patients through their clinicians or independent telemedicine providers.

Dr. Iseult Browne, a clinical oncologist based at the Royal Marsden Hospital in London and the U.K. Institute of Cancer Research, said that progress in Europe is patchier. The U.K.'s National Health Service is conducting a trial of Galleri based on data from 140,000 participants. That data will be released next year.

Browne and Reduzzi noted that inertia in the field of oncology could delay the further rollout of liquid biopsies. Oncologists have, for decades, built diagnostic and treatment plans based on data from tissue-biopsy analyses. Shaking these entrenched practices, even with data showing the utility of liquid biopsies, is difficult.

Even with single-cancer tests, Browne says that standardization is an issue. "Everyone is using a different assay," so making head-to-head comparisons to decide which test is best can be confusing. Different trials have been analyzing different markers of cancer, at various timepoints in disease progression, she said.

'Less optimistic' predictions

Ruth Etzioni, a biostatistician at Fred Hutch cancer center in Seattle, leads a multi-institute effort to review emerging cancer treatment and diagnostics. Similar to the Cancer report, Etzioni's team has modeled the impact of MCEDs and predicts that they would allow cancers to be detected at earlier stages.

However, she added, "our numbers are a little less optimistic."

The tests' helpfulness varies by cancer type, because it hinges on how long different cancers remain in each stage of progression. If a cancer lingers longer in stage I and II, then MCED tests would be well-placed to diagnose it early. But if a cancer rapidly progresses to stage IV, then the test will be less useful, Etzioni explained.

The question of how long different cancers stay in each stage is still a matter of debate. The "dwell times" used in the recent Cancer report leaned more optimistic, assuming that cancers would progress slowly enough for an annual MDEC test to make a difference.

Another reason MCED tests are not ready to replace existing diagnostics is that some analyses will always require a tissue biopsy, and current medical guidelines advise doctors to make some clinical decisions based on tumor-tissue samples.

"Immunotherapy is given in some cases based on how much your tumor has leukocytes [immune cells] infiltrating the tumor," Reduzzi said. "You cannot get that in the blood." All the researchers interviewed for this article agreed that a positive on a liquid biopsy test would need to be followed up with further testing before any cancer treatment was initiated.

So, multicancer tests may diagnose cancer earlier, but whether that early diagnosis will lead to lower death rates will depend on whether those confirmation tests happen quickly, Etzioni said. And those follow-up tests also have to be up to the task of identifying early-stage cancer, she noted.

Fixing false positives

Emerging MCEDs also have issues with false positives, Browne said. Early, non-peer reviewed data from the ongoing trial shows that Galleri was extremely good at identifying people without cancer — correctly identifying people without the disease 99.6% of the time. But meanwhile, roughly 40% of the patients that the test diagnosed with cancer were actually cancer-free.

This number of false positives puts unnecessary worry on the patient, said Browne, and each false positive could trigger follow-up tests that people would not have gotten otherwise. If scaled up to the millions of people at elevated risk of cancer, it would significantly burden any health system that adopted the tests.

To reduce false-positive rates, future studies will need to find more reliable signals of cancer to detect. Detecting information from other cell types, like immune cells, has been shown to improve test specificity. Improvements to laboratory standardization could also help cut the false-positive rate.

Browne hopes that liquid biopsy could someday help patients avoid the sapping side effects that were once unavoidable parts of cancer treatment. For instance, an ongoing trial at the Royal Marsden Hospital is assessing whether a test could identify breast cancer patients who don't need post-operative chemotherapy. The test enables the doctors to assess a patient's risk even after their tumor has been removed because it looks for tumor DNA in the blood.

Reduzzi believes that optimized multicancer tests — which would identify a large fraction of people who have cancer while having a low false-positive rate — will transform cancer diagnostics, and that such tests are on the horizon.

"I don't think we have a test that is there," she said. "But I think we will. With time."

Editor's note: This story was updated on Jan. 5, 2026, to clarify a comment from Dr. Iseult Browne and correct the name of the ongoing Galleri trial.

This article is for informational purposes only and is not meant to offer medical advice.

A new study suggests that giving immunochemotherapy earlier in the day helps patients with an advanced type of lung cancer live longer.

Previous studies suggested that the body's internal clock, the circadian rhythm, can influence how well immune checkpoint inhibitors work. These drugs help the immune system recognize and attack cancer cells by blocking tumors' ability to shut those immune responses down.

In several cancers — such as kidney, liver, stomach, esophagus, and head and neck cancers, as well as melanoma — giving this treatment in the morning has been associated with better outcomes than giving it in the late afternoon or evening.

Now, the new study, published Dec. 8 in the journal Cancer, shows that the time of day a drug is delivered also affects extensive-stage small cell lung cancer (ES-SCLC) — a fast-growing cancer that is typically associated with a poor prognosis and accounts for about 15% of new lung cancer cases.

This study is "very important," said Dr. Francis Lévi, a medical oncologist and founder of the Chronotherapy Group at Warwick University, who was not involved in the work. It extends earlier research he did with the same team, which involved different lung cancer types and different immune checkpoint inhibitors but produced similar results.

"Early time of day of immune checkpoint inhibitors, as single agents or combined with chemotherapy or antiangiogenics [drugs that starve tumors of blood], significantly improves treatment efficacy compared to later dosing times," Lévi told Live Science.

Other experts not involved in the study agreed that the results were impressive. In a joint statement, oncologist Dr. Pasquale Innominato and circadian biologist Robert Dallmann, both at Warwick University, and oncologist Dr. Seline Ismail-Sutton at the Ysbyty Gwynedd Hospital in Wales, told Live Science they were "impressed by the large effect of time-of-day of immunotherapy administration on overall survival," calling it "a very meaningful difference."

Tweaking treatment timing "represents a simple, low-cost adjustment with the potential to deliver meaningful improvements in patient outcomes … without adding new drugs or complex interventions," they said.

Earlier treatment, longer survival

In the study, researchers from the Affiliated Cancer Hospital of Xiangya School of Medicine at Central South University in China analyzed data from nearly 400 patients with ES-SCLC, a cancer with a median survival rate of 14 months. All the patients received a standard, initial immunotherapy in combination with chemotherapy between May 2019 and October 2023.

Each patient's average treatment time of day was calculated based on the first four therapy cycles. The researchers then compared survival outcomes for patients treated at different times of day, between 11 a.m. and 4:30 p.m. They matched the patients to ensure that the main thing that differed between them was the treatment timing, not baseline characteristics, such as age or sex.

3 p.m. marked a critical cutoff point. Patients who generally received treatment before 3 p.m. survived significantly longer without their cancer progressing. They also had longer overall survival over the next five years, compared with those treated later in the day.

Even after accounting for other factors that could influence the patients' outcomes, this earlier treatment time remained a strong, independent predictor of better survival.

The study findings align with laboratory studies that suggest killer T cells — immune cells that can directly kill cancer — tend to migrate into tumors in the morning, said Dr. Chi Van Dang, a professor of cancer medicine at Johns Hopkins University, who was not involved in the study. Therefore, aligning immunotherapy with this migration may help it work better, he told Live Science.

Personalized 'chronotherapy'

The large sample size of the study was a strength, but the research has some caveats.

Lévi pointed out that most patients were men, for example. The pronounced timing effects did not seem to extend to the women in the study, but this may come down to there being few women included, the study authors wrote, so it bears exploring in larger studies.

The study found that patients who received immunochemotherapy before 3 p.m. lived nearly twice as long as those treated later in the afternoon. However, this picture isn't completely clear, Lévi said, because the study doesn't pinpoint the best cutoff time for care. "This results in an uncertainty regarding the most appropriate cut off time, that actually could be located between 11:30 and 15:00," he said.

Additionally, because the study looked back at past patient data, stronger evidence will still need to come from randomized clinical trials, in which different treatment timings are explicitly tested and compared against one another. Most evidence of the benefits of early treatment "comes from retrospective studies," Innominato and colleagues said, "with only one prospective trial completed and additional trials now in development."

Assuming trials show positive results, there could still be logistical hurdles to overcome. "If treatment were restricted to a single time window, such as the morning, clinical units could quickly become overwhelmed," Innominato and colleagues said.

It's important to note that the "optimal window" for treatment may not be universal among patients, they added. It may partially depend on each individual's biological rhythms and lifestyle characteristics.

Chronotyping — categorizing people as "morning larks" or a "night owls” — could "align therapy with each patient's internal clock, accounting for individual variability and thus boosting efficacy while easing pressure on clinical units by distributing treatments across the day," they suggested. "The challenge now is to develop quick, reliable ways to identify chronotype and scale this approach, and dedicated studies are already underway."

This article is for informational purposes only and is not meant to offer medical advice.

Scientists think a very common childhood infection may be linked to bladder cancer — and now, they're figuring out the chain reaction that connects the two diseases.

It's known that people who get kidney transplants are three times more likely to develop bladder cancer than the general population. Researchers have hypothesized that because transplant patients are immunosuppressed, dormant viruses lurking in the body are given the opportunity to reactivate.

These sleeping pathogens include BK virus (BKV), also called human polyomavirus type I, a common cold virus that 95% of people pick up as children. After an infection, the virus then lies dormant in the kidney. This introduces a question: Can the BK virus cause cancer years after it infects someone?

In a study published Dec. 3 in the journal Science Advances, researchers showed that the virus can cause the type of DNA damage that is also seen in bladder cancer that occurs later in life. But instead of finding DNA mutations directly caused by the virus, the researchers found that the culprit was the body's own immune system.

"This is a nicely-done laboratory study to show a possible way that BKV could have a larger role in bladder cancer than previously thought," Dr. Patrick Moore, a tumor virology researcher at the University of Pittsburgh who was not involved in the study, told Live Science in an email.

Connecting the dots

There are several types of viral infections that can lead to cancer. Some viruses, such as HPV, hijack the host cells of the infected person and insert their viral genetic material into the human genome, which causes the host cell to become cancerous. However, in some cancers, like those originating in the bladder, no detectable virus is present —but nonetheless, there are genetic signs of a previous viral infection.

"The long-running narrative since the 1950s has been that smoking and industrial exposures are the big cause of bladder cancer," said senior study author Simon Baker, a cancer researcher at the University of York in the U.K. But the patterns of DNA mutation seen in bladder cancers are different from those resulting from chemical carcinogens.

Instead, the cancers bear mutational signatures known to be caused by a family of enzymes called APOBEC. Normally, these enzymes help form the body's first-line defense against viruses and other pathogens. "They have these signatures from APOBECs, and we know APOBECs are part of the antiviral host defense," Baker explained.

Baker and his team took healthy human bladder cells and infected them with the BK virus in lab dishes. They found that the cells not only exhibited mutations similar to those seen in bladder cancer but also boosted the activity of APOBEC3, an enzyme that damages viral genomes in response to infection.

When the scientists turned off APOBEC3 and then infected the cells with the BK virus, the DNA damage didn't occur. This finding suggests that the enzyme made by the host cell was causing the damage, not the virus itself.

Additionally, the researchers found increased APOBEC3 expression and cancer-like genetic mutations in nearby "bystander" cells that hadn't been infected with the virus. So, a cell doesn't have to contain the actual virus to accumulate genetic mutations caused by an infection elsewhere in the body.

"That was a surprise," Baker said. "But the reason it makes perfect sense is that … bladder cancers don't have viruses in them." This finding starts to unravel the connection between early-life viral infections and cancers diagnosed decades later.

A starting point

Although these initial data are impactful, Moore said he would like to see whether patients with bladder cancer are infected more often with the BK virus than people without the cancer.

"It is intriguing," he said, "but only a starting point and work needs to be done to show its actual importance to human cancer."

When a person contracts the BK virus in childhood, they generally experience common cold symptoms before recovering. The virus then stays inactive, or dormant, in the kidney, bladder and tubes between the two organs. For most people, it never becomes an issue, and it's not routinely tested for outside of hospital settings.

For those about to have a kidney transplant, however, the immunosuppressants that prevent the rejection of their new kidney can also result in the reactivation of the BK virus, possibly damaging the kidneys, ureter and bladder in the process.

Tim Tavender, a kidney transplant patient from Southampton, developed a BK virus infection following his procedure and eventually had bladder cancer.

"Seeing this research makes me hopeful," Tavender told The Independent. "If scientists like Dr. Baker can find new ways to control BK virus, it could spare other people from going through what I did — and that would be life changing."

This article is for informational purposes only and is not meant to offer medical advice.

Graying hair could be a sign that the body is effectively protecting itself from cancer, a new study suggests.

Cancer-causing triggers, such as ultraviolet (UV) light or certain chemicals, activate a natural defensive pathway that leads to premature graying but also reduces the incidence of cancer, the research found.

The researchers behind the study tracked the fate of the stem cells responsible for producing the pigment that gives hair its color. In mouse experiments, they found that these cells responded to DNA damage either by ceasing to grow and divide — leading to gray hair — or by replicating uncontrollably to ultimately form a tumor.

The findings, reported in October in the journal Nature Cell Biology, underline the importance of these sorts of protective mechanisms that emerge with age as a defense against DNA damage and disease, the study authors say.

Graying hair as cancer defense

Healthy hair growth is dependent on a population of stem cells that constantly renews itself within the hair follicle. A tiny pocket within the follicle contains reserves of melanocyte stem cells — precursors to the cells that produce the melanin pigment that gives hair its color.

"Every hair cycle, these melanocyte stem cells will divide and produce some mature, differentiated cells," said Dot Bennett, a cell biologist at City St George's, University of London who was not involved in the study. "These migrate down to the bottom of the hair follicle and start making pigment to feed into the hair."

Graying occurs when these cells can no longer produce sufficient pigment to thoroughly color each strand.

"It's a sort of exhaustion called cell senescence," Bennett explained. "It's a limit to the total number of divisions that a cell can go through, and it seems to be an anti-cancer mechanism to prevent random genetic errors acquired over time propagating uncontrollably."

When the melanocyte stem cells reach this "stemness checkpoint," they cease to divide, meaning the follicle no longer has a source of pigment to color the hair. Ordinarily, this occurs with old age as the stem cells naturally reach this limit. However, Emi Nishimura, a professor of stem cell age-related medicine, and colleagues at the University of Tokyo were interested in how this same mechanism operates in response to DNA damage — a key trigger for cancer development.

In mouse studies, the team used a combination of techniques to track the progress of individual melanocyte stem cells through the hair cycle after exposing them to different harmful environmental conditions, including ionizing radiation and carcinogenic compounds. Intriguingly, they found that the type of damage influenced how the cell reacted.

Ionizing radiation caused the stem cells to differentiate and mature, and ultimately activated the biochemical pathway responsible for cell senescence. As a result, the melanocyte stem cell reserves were rapidly depleted over the hair cycle, thus halting the production of further mature pigment cells and leading to gray hair.

Meanwhile, by essentially switching off cell division, this senescence pathway prevented the mutated DNA from passing into a new generation of cells, thus lowering the likelihood of those cells forming cancerous tumors.

Exposure to chemical carcinogens — such as 7,12-dimethylbenz[a]anthracene (DMBA), a tumour initiator widely used in cancer research — appeared to bypass this protective mechanism. Instead of switching on senescence, it toggled on a competing cellular pathway.

This alternative chemical sequence blocked cell senescence in the team's mouse studies, enabling the hair follicles to retain their stem cell reserves and the ability to produce pigment, even after DNA damage. That meant that the hair retained its color, but in the long term, the unchecked replication of damaged DNA led to tumor formation and cancer, the team said in a statement.

These findings reveal that the same stem cell population can meet opposite fates depending on the type of stress they're exposed to, lead study author Nishimura said in the statement. "It reframes hair graying and melanoma [skin cancer] not as unrelated events, but as divergent outcomes of stem cell stress responses," Nishimura added.

The next step will be to translate this understanding into human hair follicles, to see whether these observations in mice carry over to people, Bennett said.

This article is for informational purposes only and is not meant to offer medical advice.

In 1954, researchers described a new drug that sent children with acute leukemia into remission. It would become one of the first chemotherapy drugs and would later form the basis for a new, "rational" approach to designing drugs.

Gertrude Elion had earned a master's degree in chemistry in 1941, but she was turned down for many graduate research posts, which were not available to women. So she worked as a high school chemistry teacher and a food quality tester for a supermarket company, according to an autobiographical sketch she wrote in 1988.

But by 1944, she had found a job in the lab of George Hitchings at the Burroughs-Wellcome pharmaceutical company (now GSK). Hitchings was developing a novel way to make new drugs that eschewed the trial-and-error approach that had previously dominated drug design.

"One of the deciding factors may have been that my grandfather, whom I loved dearly, died of cancer when I was 15. I was highly motivated to do something that might eventually lead to a cure for this terrible disease," Elion wrote in 1988.

Hitchings and Elion reasoned that, because all living cells need nucleic acids, which make up DNA, to reproduce, then fast-growing cells, like invasive bacteria and tumor cells, would need even more of these compounds to fuel their insatiable growth. So, they rationalized, finding compounds that inhibit the synthesis of nucleic acids could squelch cancer growth.

In 1950, when Elion was 32, the team discovered a compound derived from purine, called 6-mercaptopurine (6-MP), which could inhibit the growth of both bacterial cells and leukemia cells in a lab dish. Over the next two years, they tested the drug in tumors in animals, finding that it slowed tumor growth. In 1952, researchers began trials in 107 patients with various types of cancer, including 45 children and 18 adults with acute leukemia. Prior to this, there was no good treatment for these children, who would usually die months after their diagnosis.

There had been a few earlier chemotherapy drugs, but many were based on highly toxic compounds, such as war gases. By contrast, the children who took 6-MP seemed to tolerate it fairly well, and 15 children went into complete remission for a few weeks to a few months. It wasn't a huge increase, but it was more than had been possible before. Elion was elated when the children got better, and crushed when they got sick again.

Hitchings and Elion were determined to pursue other, related compounds that could create a more durable remission. In the late 1950s, they hit upon a regimen that combined methotrexate — another chemotherapy drug, developed by Dr. Jane Wright and colleagues — with 6-MP to create a longer-lasting, stable remission in some kids with acute leukemia.

Over a decades-long career, Elion would go on to develop many more drugs, including azathioprine, a rheumatoid arthritis and transplant anti-rejection drug; acyclovir, an antiviral that treats genital herpes, chickenpox and shingles; and AZT, the first drug that worked against HIV/AIDS. In 1988, she earned the Nobel Prize in physiology or medicine, along with Hitchings and James Black for her work on "important principles in drug design," including her work on 6-MP.

Microbes in the gut can help the immune system fight cancer, and a fiber-rich diet may be the key to unlocking those benefits, a study in mice suggests.

The immune system is a key player in the body's battle against cancer. On the front line of this resistance are CD8+ killer T cells, a type of immune cell that marauds around tumors and then exterminates the cancerous cells. But after each successive battle, these cells become worn out and don't find tumors as effectively. As such, treatments that provide the cells with enough pep to finish their job are in high demand.

Now, in a study published Nov. 11 in the journal Immunity, researchers report that simple dietary changes may help revive these key immune cells by affecting the gut microbiome — the collection of microbial species in the gastrointestinal tract.

The team, led by Dr. Sammy Bedoui, an immunologist at the University of Melbourne in Australia, didn't set out to study cancer at all. Instead, their project began nearly a decade ago with "blue-sky discovery research," without a particular outcome in mind, he told Live Science.

The team was broadly exploring how CD8+ T cells defend the body. Some of their research involved mice that were genetically modified to lack gut microbiomes, and the team noticed that T cells transferred into these rodents started to die out after a couple of weeks. They began to look for a factor released by the microbiome that could help T cells thrive.

In a 2019 paper, they found that factor. When a lot of dietary fiber reaches the gut, bacteria in the colon cause the fiber to ferment. This process releases different chemicals, including short-chain fatty acids (SCFAs). Bedoui, alongside study co-author and senior research fellow Annabell Bachem, showed that a particular SCFA — butyrate — rejuvenated tired-out T cells.

"They look very much like those cells that we would like to have when we treat patients or mice with immunotherapies," Bedoui said.

Having initially shown this effect in healthy microbiota-free mice, the researchers built on this idea in their new study. They tested whether butyrate could amp up T cells in mice with the skin cancer melanoma. They put half of these mice on a high-fiber diet, which, in turn, ramped up SCFA production by their gut microbes. The mice remained tumor-free longer than mice fed a low-fiber diet, and they had smaller tumors overall; in short, the high-fiber group had slower cancer progression.

In another experiment, the team bred mice that lacked T cells and subjected them to the same protocol. Among these mice, the high-fiber diet didn't come with improved cancer outcomes, suggesting that something specific about the fiber's effect on T cells was what slowed disease progression.

The team explored how the SCFAs might be altering the mice's T cells. In the mice fed more dietary fiber, the team found more T cells specialized to fight melanoma. Specifically, these cells were seen in the tumor-draining lymph node, a staging post where T cells amass before tackling a tumor.

Importantly, these cells carried a protein that pointed to cancer-fighting prowess. "They can stay around in the body for a really long time," Bachem said of the cells. "They have the potential to get activated well, and then to differentiate into different subsets."

The team's findings differed from previous studies in that it didn't focus on the medical value of particular bacterial species, Bedoui said. No lone bug in the team's analysis contributed to the impact; it was a group effort.

"It's not so much who is there in terms of bacteria but what they are doing," Bedoui said.

These findings have opened a rich vein of future research. Bedoui and Bachem will now explore in clinical studies whether additional dietary fiber might help human melanoma patients and whether butyrate might also give other T cells their mojo back.

This article is for informational purposes only and is not meant to offer medical or dietary advice.

On Dec. 31, 2019, the first reports emerged about a mysterious pneumonia of unknown cause circulating in China. On March 11, 2020, the World Health Organization declared COVID-19 a pandemic.

On March 16, the first COVID-19 vaccine entered clinical trials.

And by Dec. 14, members of the American public were getting the first doses of COVID-19 vaccines outside of trials.

The first coronavirus vaccines were paradigm-shifting because they went from conceptualization to mass production in mere months. But they were also unique because they used a new way to stimulate the immune system — one that had been thoroughly studied for decades in order to be ready for deployment at this crucial moment.

The key to these vaccines was messenger RNA (mRNA), DNA's less-famous cousin. The power of the mRNA platform is that vaccines can be produced exceptionally quickly once a pathogen's genetics have been analyzed; conventional vaccine manufacturing takes months or years whereas mRNA vaccines can be made in mere weeks. So while it was once the subject of high school biology classes and niche pockets of biomedical science, mRNA was suddenly thrust into the public eye — and once there, it inspired relentless misinformation and controversy.

While mRNA-based COVID-19 vaccines are the best known application of the molecule, researchers around the world have found additional uses for mRNA technology beyond the realm of vaccines. They're exploring its use for groundbreaking treatments for cancer and autoimmune disease, as well as for gene-editing therapies for genetic disorders. But that promise may be unrealized in the United States, where the federal government has declared war against this promising technology.

This new stance runs counter to the Trump administration's prior embrace of mRNA vaccines.

"We do really have to give President Trump credit for introducing the mRNA platform to the world through his leadership in Operation Warp Speed," said Jeff Coller, the Bloomberg distinguished professor of RNA biology and therapeutics at Johns Hopkins University. "The president should be taking a victory lap." But instead, the second Trump administration is actively dismantling this legacy, Coller told Live Science.

Vaccine skeptic Robert F. Kennedy Jr. now heads the Department of Health and Human Services (HHS), and opponents of both conventional and mRNA-based vaccines hold seats on the country's most influential vaccine advisory committee. Since Trump's inauguration, federal scientists have faced mass layoffs, funding freezes, and memos warning them to disclose their involvement in research areas the administration has targeted, including mRNA vaccines.

These actions had an immediate chilling effect on mRNA research and development in the U.S., Coller told Live Science. And then, in August, HHS canceled nearly half a billion dollars of investment into mRNA vaccine development.

"I was shocked to see this, frankly," said Jordan Green, head of the Biomaterials and Drug Delivery Laboratory at Johns Hopkins, whose lab is developing both mRNA therapies and delivery systems to get the molecule into the body.

The cuts are sending ripples through biotech, making stakeholders question whether it's safe to set up shop in the U.S., or whether their mRNA investments would be better spent abroad. "It's just a shame because it's an unforced error; there's no reason," Green said.

For now, HHS appears to be retreating primarily from mRNA vaccines; it noted "other uses of mRNA technology" would not be affected by the cuts. But "the industry doesn't trust that," Coller told Live Science.

According to Grant Witness, a project tracking scientific grants under the Trump administration, mRNA research unrelated to vaccines has already been hit by grant terminations and funding freezes. So even if it's not being explicitly targeted, it's not necessarily being preserved. The project's database shows that the National Institutes of Health (NIH), part of HHS, terminated grants for projects developing mRNA-based treatments for cancer, Alzheimer's, pulmonary arterial hypertension and HIV, as well as grants for basic research about how mRNA works in healthy and diseased cells.

Here's what the United States stands to lose if the federal government broadly divests of mRNA medicines after spending decades readying the technology for prime time.

Cancer treatment

On a molecular level, mRNA is a close cousin of DNA — and human cells are stuffed with it. These ubiquitous "messengers" copy instructions from DNA and relay them to other locations in the cell — namely, to protein-construction sites where the complex molecules that do most of the work in cells get made. mRNA also performs other key jobs in cells, such as helping control which genes are switched on and to what degree.

For decades prior to the pandemic, dedicated scientists pored over mRNA, learning how this class of molecules works in the body and how it might be leveraged to heal the sick and guard against disease.

"I started doing this when I was like 21, back in the '90s, back when about 10 people on Earth knew what mRNA were," Coller said. Findings from Coller's lab later helped inform the development of Spikevax, the COVID-19 vaccine made by Moderna. But while COVID-19 vaccines are the best-known application of mRNA to date, they're far from the first.

The first mRNA therapeutics company was founded in 1997, and rather than targeting infectious disease, it had its sights set on cancer treatment. Its approach ultimately hasn't panned out in human trials, but in the meantime, other approaches to mRNA-based cancer treatment have gained traction.

Cancer vaccines are a standout example, but in this context, the term "vaccine" is "a bit of a misnomer," said Dr. Vinod Balachandran, a pancreatic cancer surgeon-scientist and director of The Olayan Center for Cancer Vaccines (OCCV) at Memorial Sloan Kettering Cancer Center. Rather than being given preventatively, like a COVID vaccine, cancer vaccines are "given to patients as a treatment; it is a therapy," he said.

These therapies are similar to conventional vaccines in that they train the immune system to recognize antigens, which are substances that act as "red flags" for foreign invaders, toxins or diseased cells. These include, for example, the spike protein of SARS-CoV-2 — the virus that causes COVID-19 — and certain molecules on cancer cells. Balachandran and colleagues have focused on pancreatic cancer, which has a five-year relative survival rate of only 13% — meaning people newly diagnosed with pancreatic cancer are about 13% as likely to survive the next five years compared with the general population.

The researchers have found that, in the rare long-term survivors of pancreatic cancer, the immune system can recognize the cancer and fight off its recurrence. The team hoped to re-create that immune recognition in other patients by analyzing the genetics of their tumors to see what unique antigens they express. They then create customized vaccines that target those molecules.

"We felt at the time [when we started this work] — this is back in 2017 — that the best technology for rapid custom cancer vaccination for patients was to use RNA," Balachandran said. Once you know a given patient's cancer genetics, a personalized mRNA vaccine that targets multiple antigens can be crafted in a matter of weeks. Conventional vaccines that require the antigens to be grown in the lab and purified would take many months to make.

"For cancer vaccination, speed is essential," Balachandran said. "These are patients who are facing deadly cancers, who require rapid treatment. So we do not have the luxury of waiting."

So far, the team has seen some success. In an early-stage trial, they treated 16 patients who had undergone surgery for pancreatic ductal adenocarcinoma (PDAC), the most common form of pancreatic cancer, which has a five-year survival rate of about 10% to 12%, though they fare a bit better when their cancer can be surgically removed.

Within nine weeks of surgery, Balachandran said, each patient's tumor tissue was analyzed and a personalized vaccine was crafted and delivered alongside post-surgery cancer treatments, like chemotherapy. Half of the patients responded to their vaccine, producing immune cells that have persisted for nearly four years so far, and estimates suggest they could last an average of seven years, "with some lasting even beyond a decade," Balachandran said.

The vaccine responders had a significantly lower risk of recurrence in the following three years than those who didn't respond, with six showing no signs of recurrence in that time frame. A mid-stage trial is now testing the vaccine in about 260 people to see how well it delays or prevents recurrence compared with standard treatment.

"Anything we can do to improve outcomes for these patients who really need help I think will be transformative for the field, for them, for their families — it will mean a lot," Balachandran said. "All other immune therapies and all other therapies have largely failed."

In this initial trial, vaccine production took over two months, in part because samples had to be shipped to overseas collaborators at BioNTech. "We are confident this can happen much faster" in the future, perhaps within a month, Balachandran said.

Other scientists are working on off-the-shelf cancer vaccines that can help bridge the gap until a patient gets a personalized one. These vaccines use a mix of mRNA molecules to stir up a generic, first-line immune defense against cancer. In mice with different kinds of solid tumors, researchers led by Dr. Elias Sayour, a pediatric oncologist at the University of Florida, demonstrated that such a vaccine triggers anti-cancer responses by itself. And when used in combination with another cancer treatment, the mRNA mix can boost the effects of that therapy, Sayour's team has found.

That team has now moved on to human patients, with a two-pronged approach: an off-the-shelf cancer vaccine, followed by a personalized one. They have also run trials of personalized vaccines for the deadly brain cancer glioblastoma, finding that the shots mount a strong, targeted immune response against these tumors that are usually difficult for the immune system to "see." Meanwhile, at another lab, scientists are testing a personalized vaccine in late-stage trials for the skin cancer melanoma and non-small cell lung cancers.

Pancreatic cancer has historically been an elusive target for the immune system because, compared to cancers like melanoma, its cells carry relatively few antigens, Balachandran explained. But pancreatic cancer can be targeted with these vaccines. That bodes well for using mRNA approaches to treat potentially many other cancers, and "I think that's really the most exciting take-home," he said.

Beyond cancer vaccines, Green and colleagues are leveraging mRNA to fight the disease in a different way: by forcing tumors to raise their own red flags to the immune system. Using mRNA packaged inside nanoparticles, the researchers introduce immune-cell genes into cancer cells, prompting tumors to expose their antigens and secrete molecules that call immune cells to the area.

"We can program that tumor cell to now act like an immune cell that helps teach other immune cells what its antigens look like, how to recognize it, how to destroy it," Green told Live Science. In mouse models of breast cancer and melanoma, they combined this approach with an existing immunotherapy and found that it helped shrink and clear tumors from the body while also extending survival.

If shown to work in people, "this could just be off the shelf," he said. It would be one injectable that could work on any patient's solid tumor, he said.

Immune reprogramming

In cancer, scientists are exploring different ways to launch an immune attack against tumor cells, whether by igniting a generalized response or enabling cells to spot specific red flags. But in some diseases, the immune system itself is the culprit — and in those instances, mRNA can help rein in turncoat immune cells.

"Autoimmune diseases — type 1 diabetes, multiple sclerosis, Crohn's, colitis — these can be treated with these mRNA and genetic-based therapies," potentially, Green said. The goal of these treatments would be to "tune the immune system" so it stops attacking healthy tissues.

In type 1 diabetes, for example, the immune system attacks beta cells, which make insulin, leaving the body too little of the hormone to control blood sugar. Green and colleagues are in the early stages of developing an mRNA medicine to reprogram the immune system so it better tolerates beta cells, rather than attacking them. They aim to do this by targeting special immune cells in the liver that promote a tolerant environment in the organ.

The liver is constantly exposed to antigens from food and from microbes in the gut, so immune activity is dialed down to prevent an overreaction. The team's idea is to deliver mRNA that codes for beta-cell proteins to the liver, essentially marking those beta-cell proteins as "safe" to the immune system. This, in turn, can increase the number of regulatory T cells that recognize the proteins as safe; regulatory T cells keep other immune cells in check, and could thus help ward off further attacks on beta cells.

"The problem with autoimmunity is that [the immune system] thinks parts of its own body are foreign," so it's trying to attack them, Green explained. The hope is that "we can use these mRNA medicines to train the immune system so that it sees, 'Oh no, this is fine.'" The work is currently in preclinical stages, as the team runs experiments with cells and lab mice to refine their mRNA nanoparticles.

Green calls this approach of fine-tuning specific cells' activity "genetic surgery." Rather than using a "blunter instrument," like immunosuppressive drugs, to broadly suppress the immune system, the surgery makes a precise change to counter only harmful immune activity. In the long run, the lab is looking to apply this same approach to other autoimmune diseases beyond diabetes, such as multiple sclerosis, in which immune cells target myelin, the insulation surrounding nerve fibers in the brain and spinal cord.

Meanwhile, BioNTech has published data from its own early tests of an mRNA vaccine designed to quell autoimmunity against myelin. In mice, the vaccine expanded populations of immune cells that then kept the myelin-attacking cells in check, suppressing their activity without hobbling the immune system as a whole.

Elsewhere, researchers including Dr. Samira Kiani of the University of Pittsburgh School of Medicine and Kathryn Whitehead of Carnegie Mellon University are using mRNA to counter off-the-rails immune responses, such as the extreme inflammation seen in sepsis. Their approach, described in a preprint, packages mRNA inside a tiny bubble of fat called a lipid nanoparticle (LNP), which then ferries the mRNA into immune cells. From there, the mRNA instructs the cells to make proteins called "zinc finger repressors," which latch onto genes and suppress their activity. In this case, they repressed a key gene involved in the immune signaling that can lead to runaway inflammation.

In experiments with cells in lab dishes and with mice, this type of "epigenetic engineering" showed promise as a potential method for tuning the activity of the immune system. One perk of mRNA is that it degrades quickly in the body, the study authors wrote, so in theory, once the harmful inflammation is subdued, the immune system can get back to defending the body against germs.

Gene editing

mRNA is also being used in tandem with the gene-editing system CRISPR to revolutionize treatments for genetic disease.

Classical CRISPR systems use molecular scissors to snip through DNA strands and enable scientists to tweak specific segments of the molecule. And now, a modified system called base editing can be used to precisely change just one "letter" in DNA's code.

But if you want to use CRISPR for gene therapy, you must first get the scissors, as well as a "guide" molecule that directs them to the right spot — into human cells. And, ideally, the scissors enter only the cells you need to edit, said Giedrius Gasiūnas, a senior researcher in the Life Sciences Center at Vilnius University in Lithuania.

That's where mRNA packaged in nanoparticles could be a game changer.

"This technology could be important for in vivo delivery," meaning the delivery of gene editors directly into the body, said Gasiūnas, who is also chief scientific officer of the biotech company Caszyme.

The first CRISPR-based therapy approved in the U.S. involved editing cells outside the body. The therapy treats two blood disorders by disabling a gene called BCL11A; patients have blood-making stem cells removed from their bone marrow, edited in the lab and then returned to their bodies. But this complex treatment involves a month-long hospital stay, during which the edited stem cells give rise to new blood cells. By comparison, mRNA approaches to gene therapy would be easier to administer and thus more likely to be scalable, Gasiūnas said.

mRNA isn't the only vehicle for getting CRISPR therapies into the body. Some existing gene-editing treatments instead use harmless viruses, such as adeno-associated virus (AAV) vectors, and this same approach is being applied to CRISPR in some emerging therapies. But mRNA packaged inside nanoparticles is emerging as a key player in the field.

This application made headlines in the case of KJ, an infant who became the first person to receive a personalized CRISPR treatment. "The CRISPR technology was introduced as an mRNA," Coller said. "That is the critical feature that was necessary to get this to work."

KJ was born with a severe form of carbamoyl phosphate synthetase 1 (CPS1) deficiency, an inherited disease that causes ammonia to accumulate in the body and affects an estimated 1 in 1.3 million people worldwide. The condition arises from mutations in the CPS1 gene, but in different patients, the gene is broken in different ways. To fix KJ's specific mutation, scientists developed a customized gene therapy consisting of a guide and an mRNA that carried instructions for a base editor into his liver cells, where CPS1 is most active.

"The editor is so large that it cannot easily be accommodated by an AAV vector," said Dr. Kiran Musunuru, co-developer of the therapy and a professor at the University of Pennsylvania's Perelman School of Medicine. Because other potential delivery systems are too early in development, "LNPs are currently the best option," Musunuru told Live Science in an email.

The therapy was ready to administer within six months of KJ's birth. By 9 months old, he had received several doses of the therapy and was thriving; he was hitting milestones he may have never reached otherwise, his medical team reported in May. Had he not received the treatment, he would have needed a liver transplant once he got big enough.

Promising technology at risk

When it comes to the future of mRNA medicines in the U.S., vaccines for infectious disease currently have the bleakest outlook due to political barriers being raised around the technology. Among mRNA tech, vaccines have been the primary target of the federal government's ire, despite experts' warnings that abandoning the shots will leave us vulnerable to pandemics.

"It's foolish to condemn mRNA because people didn't like vaccine mandates or mask mandates or whatever they didn't like," Dr. Seth Berkley, an epidemiologist and senior adviser to the pandemic center at the Brown University School of Public Health, told Live Science. "What we need to do is improve upon them [mRNA vaccines] and understand what the best use of them is," which can only be accomplished through investing in further research.

For now, other applications of mRNA don't appear to be a focus for funding cuts, although some projects have nonetheless been caught in the crosshairs of reduced federal spending. For his part, Musunuru told Live Science he's been in discussions with the Food and Drug Administration regarding ways to get more patients access to personalized gene therapies like KJ's, so that the technology isn't used only in a handful of special cases. When asked about potential funding cuts, he added, "Vaccines and therapies are so different that I do not expect the latter to be affected."

Green, however, anticipates that divestments from vaccines would have unanticipated impacts across the field, because mRNA therapies and vaccines are ultimately composed of very similar genetic molecules and delivery systems.

Regarding nanoparticles, "the vaccine development is … at the pioneering edge of this technology platform," Green said. He argues that cuts to vaccine R&D will inevitably undermine the development of nanoparticles that could be really useful in treating cancer or genetic disease. "It's going to set us back in a very broad way," he said.

The hits to vaccine research also aren't happening in isolation. Myriad federal science grants have been terminated or frozen; NIH agencies may be facing steep funding cuts; and the government shutdown ushered mass layoffs across leading health institutions. Sayour, the oncologist whose lab is developing personalized and universal cancer vaccines using mRNA, said federal grants have historically been critical to his research.

"None of this would be possible without the support of the federal government," Sayour told Live Science. "That is most certainly, 100% true." And that goes for every stage of research, from studies in lab dishes to large clinical trials.

These widespread cuts and more-targeted cuts to mRNA vaccines will not only starve the academic environments where new biotechnologies are typically nurtured, Coller said; they will also drive prospective talent, investors and industry stakeholders in the mRNA space away from the U.S. "In biotech, we're going to see, over the next five to 10 years, a significant 'brain drain,' where other countries build up their infrastructure," he said.

Coller knows this because he is a founding member of the Alliance for mRNA Medicines (AMM), a global organization aimed at advancing and advocating for mRNA medicines. In the spring, AMM surveyed over 100 leaders in the field. They primarily represented U.S.-headquartered pharmaceutical and biotechnology organizations but also included some based in Europe, Canada or Asia. Even prior to the major HHS cuts in August, these stakeholders were feeling squeezed; nearly half reported "already experiencing direct impacts" from federal policy changes tied to mRNA funding.

The cuts caused projects to be scaled back, partnerships to be terminated, and jobs to be lost. About 30% of respondents said that, if faced with further cuts, they might pivot away from mRNA, and 30% said they'd consider moving their operations to other countries. Over 80% agreed that anti-mRNA policies would drive talent away from the U.S. and toward other locales.

Even as scientists contend with these big-picture problems on the national and international stage, skirmishes have also been unfolding at the state level. These battles primarily concern public access to mRNA vaccines but could potentially have broader ripple effects.

A bill still in committee in Iowa would make administering an mRNA vaccine in the state a misdemeanor with a fine of $500 for each shot given. Another bill in committee in South Carolina would prohibit the use of mRNA-based "gene therapies" in the state, but makes an exception for therapies for noninfectious diseases, such as cancer.

It may be that most bills of this ilk never become law and some, like the one raised in South Carolina and two dead bills in Texas, purposely make exceptions for certain uses of mRNA. However, others have been worded in ways that made it unclear whether any mRNA medicine is permissible. If any of such bills ultimately pass at the state level, that could sway where mRNA companies can manufacture products and run clinical trials, Coller said. So, while an exodus of expertise unfolds at a national level, we may see an echo of that at the state level.

The future of mRNA medicine in the U.S. rests on many "ifs," and the worst-case scenario may not come to pass. But in the face of staggering uncertainty, researchers in the field are starting to look for better bets.

"Let's not fool ourselves: mRNA is one of the three most important molecules in the body, with the other two being DNA and protein. It's the intermediary between them," Coller said. "When the federal government sends a message that mRNA-based medicine and research is not wanted, you're basically saying that there's a whole branch of science that is no longer welcome within the U.S."

"Chemo brain" — chemotherapy-induced difficulties with focusing, thinking and remembering — may be caused by the cancer treatment's disruption to the brain's lymphatic system, an early-stage study suggests.

The study zoomed in on the meningeal lymphatics, the drainage network found in the protective tissue layer surrounding the brain. Dysfunction in this network has been linked to Alzheimer's disease, Parkinson's disease and traumatic brain injuries.

Now, the new research, published Oct. 13 in the journal Communications Biology, has linked damage to the meningeal lymphatics with the brain fog that patients commonly experience after receiving chemotherapy.

Using human and mouse cells, as well as living lab mice, researchers found evidence that a common type of chemotherapy drug that blocks cancer cells from dividing, called taxanes, damages the brain's lymphatic vessels and limits their drainage. Normally, the vessels would work together with the brain's glymphatic system to flush away metabolic waste.

"Lymphatic health really declined across all three models measured in different ways," study co-author Jennifer Munson, director of Virginia Tech's Cancer Research Center in Roanoke, Virginia, said in a statement. The vessels shrank and had fewer branches, which "are signs of reduced growth that indicate the lymphatics are changing, or not regenerating in beneficial ways," she said.

"Chemo brain" is a broad category of cognitive changes that follow chemotherapy and can last for years after treatment. "There's really a lot we don't know," Munson told Live Science, but these cognitive impairments have previously been linked to oxidative stress and inflammation, as well as impaired myelin production. (Myelin is fatty insulation that covers nerve fibers.)

"Others had looked on the neural side, so we wanted to focus on the meningeal side," Munson said.

To do this, Munson and her team used three models — human cells, mouse tissues and live mice — to assess whether chemotherapy drugs led to changes to the meningeal lymphatics at different scales.

First, they used cell lines to build a human-cell model of healthy meningeal lymphatics. This model paired cells from the lining of lymphatic vessels with meningeal cells. This enabled the team to tease apart the isolated effects of chemo on each cell's function. They also grew healthy mouse meningeal tissue in lab dishes to assess any structural changes triggered by the drug exposure.

They found that the drug docetaxel disrupted the cells in the human meningeal lymphatic model by reducing their coverage and length. The treatment also shrank the vessels within the mouse tissues and reduced the number of loops in the network structure.

Next, the researchers ran experiments with live mice, comparing mice treated with docetaxel to mice unexposed to the drug. Mice with cancerous tumors that were given the drug tended to have narrower meningeal lymphatic vessels, as well as fewer loops, compared to untreated mice.

The researchers wanted to see whether these docetaxel-induced structural changes led to impaired memory or changes in behavior. They found that healthy mice treated with docetaxel forgot objects they had previously seen, while the untreated mice showed clear signs of remembering them. MRI scans of the treated mice indicated that these cognitive issues correlated with the decreased flow of fluids through the lymphatic vessels, the authors wrote in the study.

Munson cautioned that this is an early-stage study and that there are many gaps left in our understanding of the link between "chemo brain" and meningeal lymphatics. She explained that one limitation of the research was that the chemotherapy drugs were administered over relatively short time periods, whereas chemotherapy courses for human cancer patients often last months.

Similarly, the memory issues the mice experienced were tested over a couple of days, whereas humans can sometimes experience chemo brain for years following treatment. "So it's possible that these lasting effects that we see in [human] patients may have different mechanisms that may not be captured fully here," Munson said.

It is important to replicate this research using samples from many individuals of different ages and to compare outcomes between tumor-bearing and tumor-free mice, to see if there's a difference in how the chemotherapy affects them, Munson said. She hopes that, eventually, this research will provide a new target for treating this side effect of chemotherapy.

"Ultimately, this work underscores the need to consider not only survival, but also the long-term, often overlooked neurological side effects of cancer treatment on cognitive well-being and quality of life," study co-author Monet Roberts, an assistant professor of biomedical engineering and mechanics at Virginia Tech, said in the statement.

This article is for informational purposes only and is not meant to offer medical advice.

The COVID-19 mRNA-based vaccines that saved 2.5 million lives globally during the pandemic could help spark the immune system to fight cancer. This is the surprising takeaway of a new study that we and our colleagues published in the journal Nature.

While developing mRNA vaccines for patients with brain tumors in 2016, our team, led by pediatric oncologist Elias Sayour, discovered that mRNA can train immune systems to kill tumors — even if the mRNA is not related to cancer.

Based on this finding, we hypothesized that mRNA vaccines designed to target the SARS-CoV-2 virus that causes COVID-19 might also have antitumor effects.

So we looked at clinical outcomes for more than 1,000 late-stage melanoma and lung cancer patients treated with a type of immunotherapy called immune checkpoint inhibitors. This treatment is a common approach doctors use to train the immune system to kill cancer. It does this by blocking a protein that tumor cells make to turn off immune cells, enabling the immune system to continue killing cancer.

Remarkably, patients who received either the Pfizer or Moderna mRNA-based COVID-19 vaccine within 100 days of starting immunotherapy were more than twice as likely to be alive after three years compared with those who didn't receive either vaccine. Surprisingly, patients with tumors that don't typically respond well to immunotherapy also saw very strong benefits, with nearly fivefold improvement in three-year overall survival. This link between improved survival and receiving a COVID-19 mRNA vaccine remained strong even after we controlled for factors like disease severity and co-occurring conditions.

To understand the underlying mechanism, we turned to animal models. We found that COVID-19 mRNA vaccines act like an alarm, triggering the body's immune system to recognize and kill tumor cells and overcome the cancer's ability to turn off immune cells. When combined, vaccines and immune checkpoint inhibitors coordinate to unleash the full power of the immune system to kill cancer cells.

Why it matters

Immunotherapy with immune checkpoint inhibitors has revolutionized cancer treatment over the past decade by producing cures in many patients who were previously considered incurable. However, these therapies are ineffective in patients with "cold" tumors that successfully evade immune detection.

Our findings suggest that mRNA vaccines may provide just the spark the immune system needs to turn these "cold" tumors "hot." If validated in our upcoming clinical trial, our hope is that this widely available, low-cost intervention could extend the benefits of immunotherapy to millions of patients who otherwise would not benefit from this therapy.

What other research is being done

Unlike vaccines for infectious diseases, which are used to prevent an infection, therapeutic cancer vaccines are used to help train the immune systems of cancer patients to better fight tumors.

We and many others are currently working hard to make personalized mRNA vaccines for patients with cancer. This involves taking a small sample of a patient's tumor and using machine learning algorithms to predict which proteins in the tumor would be the best targets for a vaccine. However, this approach can be costly and difficult to manufacture.

In contrast, COVID-19 mRNA vaccines do not need to be personalized, are already widely available at low or no cost around the globe, and could be administered at any time during a patient's treatment. Our findings that COVID-19 mRNA vaccines have substantial antitumor effects bring hope that they could help extend the anti-cancer benefits of mRNA vaccines to all.

What's next

In pursuit of this goal, we are preparing to test this treatment strategy in patients with a nationwide clinical trial in people with lung cancer. People receiving an immune checkpoint inhibitor will be randomized to either receive a COVID-19 mRNA vaccine during treatment or not.

This study will tell us whether COVID-19 mRNA vaccines should be included as part of the standard of care for patients receiving an immune checkpoint inhibitor. Ultimately, we hope that this approach will help many patients who are treated with immune therapy, and especially those who currently lack effective treatment options.

This work exemplifies how a tool born from a global pandemic may provide a new weapon against cancer and rapidly extend the benefits of existing treatments to millions of patients. By harnessing a familiar vaccine in a new way, we hope to extend the lifesaving benefits of immunotherapy to cancer patients who were previously left behind.

This edited article is republished from The Conversation under a Creative Commons license. Read the original article.

Happiness is known to correlate with better health. But now, researchers have identified a happiness threshold above which people are less likely to die prematurely of chronic diseases like cancer, diabetes and heart disease.

By comparing data from 123 countries over 15 years, researchers pinpointed a threshold at which mortality declined as well-being increased. Every incremental improvement in well-being above this level was tied to a corresponding drop in the risk of death.

Cancer, heart disease, asthma and other chronic diseases accounted for 75% of non-pandemic related deaths in 2021, according to the World Health Organization (WHO). In the U.S., they're collectively the leading causes of illness, disability and death.

Overall chronic disease mortality decreased in the U.S. between 2010 and 2019, but its prevalence increased among Americans ages 20 to 45 years old, according to a study published in The Lancet earlier this year.

A tipping point

Although previous research assumed a positive association between happiness and health, the goal for this new study, which was published Monday (Oct. 20) in the journal Frontiers of Medicine, was to identify a tipping point at which a higher level of well-being would be associated with measurable health improvements — namely, a reduction in premature deaths due to chronic disease.

To do that, the researchers looked at yearly happiness scores in 123 countries, which they averaged to estimate the national level of subjective well-being.

Related: Can faking a smile make you feel happier?

Respondents from the happiness datasets used in the study were asked to visualize a ladder, with the top representing the best possible life and the bottom the worst. They were then asked to rate their present satisfaction and assess their future on a scale of 0 (bottom of the ladder) to 10 (top of the ladder). This tool, known as the Cantril's life ladder scale, is a well-known social science tool used to gauge life satisfaction.

Researchers then compared this measure of national well-being with chronic disease mortality rates in each country over a period of 15 years (2006 to 2021).

The study identified a happiness threshold of 2.7 on the life ladder scale. Above that threshold, every 1% increase in happiness was associated with a 0.43% decrease in premature deaths from chronic disease.

The average life ladder score among the 123 countries studied was 5.45 between 2006 and 2021, so a 2.7 score suggests participants were "barely coping," study co-author Iulia Iuga, a professor at 1 Decembrie 1918 University in Romania said in a statement.

Health effects of subjective well-being

Although the new study doesn't establish a strict cause-and-effect relationship, scientists have identified several ways well-being could have health benefits.

For one, happiness could reduce the impact of stress, which is strongly associated with the development of many chronic diseases.

"We find that positive emotion can serve as a buffer for stressful experiences," said John Hunter, an assistant professor of psychology at Chapman University in California who was not involved in the research."When you have more positive emotion, you have less stress reactivity, which means that when a stressor hits you, you react less severely," Hunter said. "Your heart rate spikes a little bit less; your blood pressure spikes a little bit less. The way that you release stress hormones also changes."

In addition, people with higher levels of positive emotion often maintain stronger relationships and healthier habits.

"People who are optimistic, people who are happy, people who have a more dynamic, happy social life, people who have a strong sense of life purpose [...] tend to be more proactive about their health," said Dr. Alan Rozanski, a cardiologist and professor of medicine at the Icahn School of Medicine at Mount Sinai who was not involved in the study. "They tend to exercise more. They tend to have better diets. They tend to sleep better."

A useful tool for policymakers

The new study could help policymakers think of happiness as a "public health resource" and use it alongside other key factors to mitigate the impact of chronic diseases on their population, the study authors said in a statement.

Policymakers should aim to push their population’s average well-being above the Cantril threshold while addressing trends and environmental conditions that can worsen chronic conditions, such as obesity, alcohol consumption and pollution, Iuga told Live Science in an email.

In places where well-being is lower, focusing on financing healthcare and improving governance is necessary to unlock the positive health effects of increased happiness, Iuga added.

Because the well-being data used in this study is self-reported, it could be subject to measurement errors, the study noted. In addition, various cultures might assess their level of subjective happiness differently.

The life ladder scale used in this study could also be interpreted as a measure of status rather than emotional happiness, Hunter said. So the question may be capturing people’s economic state and living conditions, rather than their emotional state, he said.

Around four years ago, now 77-year-old John Gormly went for what was supposed to be a routine blood test. But the results were life-changing.

The test suggested Gormly had colon cancer, which a colonoscopy later confirmed was Stage 2, meaning the cancer had spread through the wall of the colon but not to his lymph nodes.

"I thought [my doctor] was wrong," Gormly, CEO of a construction company near Newport Beach, California, told Live Science. "I go, 'Nah, I don't feel anything.' But there it was. It was real; the colonoscopy showed it."

Gormly was one of the first patients to take a newly approved test called Shield, which its makers say can detect colon cancer from a blood sample. After his diagnosis, Gormly had surgery to remove the tumor and was back to work within 10 days.

An early version of Guardant Health's Shield test has been commercially available since 2022, but it wasn't covered by insurance. However, after approval from the U.S. Food and Drug Administration (FDA) in July 2024, a diagnostic version of Shield was launched commercially and is now covered by Medicare.

Shield is only a blood drop in an ocean of emerging "liquid biopsies."

Scientists have developed blood tests for several cancers, including those of the breast, pancreas and stomach. Some blood tests even detect multiple types of cancer. If these liquid biopsies can be rolled out widely, they could help detect cancer earlier, more easily, or with fewer invasive measures — which, in turn, could lead to earlier detection and fewer cancer deaths.

But many of these tests are still in their early stages. They often detect a lower fraction of cancer cases than gold-standard screening tools like colonoscopies do, meaning they will likely supplement, rather than replace, traditional screening methods. Others may have unacceptable rates of "false positives," meaning a person is initially told they have cancer but diagnostic follow-ups show they do not. This can lead to needless worry or additional invasive tests. These include traditional biopsies, which involve removing tissue samples via needles or surgery. And for some diseases, it's not clear that early diagnosis on a blood test will lead to better outcomes.

However, as these kinks are ironed out, it's likely that blood-based cancer screening will become a normal part of our medical care — one that has the potential to improve cancer outcomes dramatically, experts say.

Simplifying screening

Gormly's doctor recommended a Shield test after noticing that Gormly hadn't had a colonoscopy in a while. He's not alone. Current recommendations suggest that people ages 45 to 75 who are at average risk of colon cancer get a screening, such as a colonoscopy or a stool-based test, every five to 10 years. Yet around 1 in 3 of these people have never been screened.

That's a problem, because colon cancer is the fourth-most-common cancer. Experts have argued that early detection could eliminate 90% of colon cancer deaths. It typically takes around 10 years for early, precancerous growths like polyps to morph into deadly cancer cells, and if these cells are caught early, they can easily be removed.

Despite the potential for early diagnosis and cure, many people avoid these screenings. This may be one reason colon cancer is the second-most-common cause of cancer death.

People avoid screenings for many reasons, said Dr. William Grady, a professor of translational science and therapeutics at the Fred Hutchinson Cancer Center in Seattle who helped lead the Shield trials. Some people feel embarrassed during screenings such as colonoscopy or fear that it may be painful, he told Live Science. Those opting for colonoscopy may struggle to get time off work, whereas others may dislike the idea of handling stool for a stool-based test, he said.

"That's why there's an opportunity for blood tests that is really powerful because people are inclined to do blood tests; they're convenient and can be done during a health care encounter," Grady said.

Shield works by detecting small DNA fragments that are released into the blood from colon cancer cells or precancerous cells called adenomas, a type of polyp. The test also picks up on subtle differences between cancerous cells and normal cells in chemical tags on DNA known as methyl groups.

In a paper published in March 2024 in The New England Journal of Medicine, Grady's team showed that Shield detected 83% of colonoscopy-confirmed colon cancer cases in a cohort of almost 10,000 people. It also had a false positive rate of 10%.

Because Shield detects a smaller percentage of colon cancer cases than stool-based tests (92%) or colonoscopies (95%) do, it won't replace those diagnostic tests, Grady said. However, it could expand the number of screening options available to patients, he added. This additional option may improve screening compliance, which could lead to earlier disease detection and thus a reduction in colon cancer deaths.

The Shield test is approved for use every three years, Grady said. However, current studies are investigating whether it would be more accurate if it were done every year or two, he added.

If Gormly's cancer had spread to the rest of his body, it would have been much harder to treat. People whose colon cancer is caught at Stage 2, like Gormly, have an 85% chance of living at least another five years. By Stage 4, when it has spread throughout the body, those odds go down to just 10%.

"That could have been the end of me, so it [Shield] definitely changed my life," Gormly said.

Accelerating diagnosis

Pancreatic cancer is another disease that could benefit from a blood-based diagnostic test. Unlike colon cancer, pancreatic cancer is relatively uncommon, affecting 1 in 56 men and 1 in 60 women. Yet pancreatic cancer is the third-most-common cause of cancer death in the U.S.

That's because, by the time most people notice symptoms, such as abdominal pain or discomfort, the disease is already very advanced, said Ajay Goel, a professor and chair of the Department of Molecular Diagnostics and Experimental Therapeutics at the Beckman Research Institute of City of Hope in Duarte, California.

There is no broad-based screening program in the U.S. for people at average risk of pancreatic cancer. Later stages of the disease are easily detectable via MRI or CT scan, Goel told Live Science. But by that point, the five-year survival rate is extremely low: around 3% once the cancer has spread throughout the body, compared with 44% if it is still limited to the pancreas. Once cancer has spread beyond the pancreas, surgical removal is usually no longer possible, and treatments such as chemotherapy and radiotherapy are minimally effective.

A potential solution is a new blood test developed by Goel's team. It aims to detect early-stage pancreatic cancer by identifying small cancer-specific molecules called microRNAs. These molecules regulate whether genes are switched on or off and are found in the blood of patients with early-stage disease, as well as inside exosomes, which are tiny packages that cancer cells release into the blood.

In a study of nearly 1,000 people, the test (which is still unnamed) detected between 88% and 93% of early- and late-stage pancreatic cancer cases, using blood drawn from people in the U.S., South Korea and China. When the test was modified to also measure the amount of a protein known as CA-19 in the blood, it picked up 97% of early-stage cases in the U.S. group. CA-19 is a known biomarker of pancreatic cancer, but on its own, it is not reliable enough to be used for diagnosis. When combined with CA-19 detection, the new test had a 5% to 10% false positive rate, Goel said.

The findings, which haven't been peer-reviewed yet, were presented at the 2024 American Association for Cancer Research Annual Meeting in San Diego.

"If you can find more and more of these cancers early on, there is a hope that many of these patients can be cured," Goel said.

The team envisages the test being taken yearly — for instance, when patients see their doctor for an annual physical exam. However, in those who have a family history of pancreatic cancer, it may make sense to test more frequently — perhaps every six months, Goel said.

Multicancer detection

Scientists are also developing multicancer detection (MCD) tests that screen for many types of cancer at once. MCD tests differ slightly in the types of cancer they detect and how they do it. But like many of the single-cancer detection tests, MCD tests look for cancer-specific molecules, such as tumor DNA, but on a larger scale. Some MCD tests sample urine or another bodily fluid in addition to blood.

In theory, such tests could not only provide a less-invasive approach to screening but also reduce the number of tests a person has to take at once. However, most of these tests are still in early development. The ones that are farther along, such as Grail's Galleri and Exact Sciences' Cancerguard, have not received FDA approval yet. And some experts have argued that the tests' efficacy claims are overhyped.

Even if MCD tests do work and they become more affordable (Galleri, for example, currently costs around $950), experts still aren't sure of the best way to use them. "There's this belief that if we could only detect all cancers early, we would solve the cancer problem," Ruth Etzioni, a professor at Fred Hutchinson who was not involved in Grady's work with Shield, told Live Science. But sometimes there is no good treatment for early cancers, so catching them ahead doesn't necessarily lead to improved outcomes.

And there's always a risk of false positives. After taking an MCD test, patients may wait up to six months to know one way or the other, Dr. Jennifer Croswell, a medical officer at the National Cancer Institute, told Live Science. There may be many reasons for this delay, including that it takes time to perform multiple rounds of follow-up testing to figure out which organ is affected, she said. There are also currently no evidence-based clinical guidelines that tell doctors the best way to follow up on positive results from MCD tests, Croswell said. Consequently, these tests may create uncertainty for patients.

The way forward

While many diagnostic blood tests for cancer are still in the pipeline, at least some of these tests will likely affect diagnosis and treatment in the next several years. For instance, Goel and colleagues are now running a clinical trial to see if their test can detect early-stage pancreatic cancer in high-risk individuals who have not yet been diagnosed. If it's successful, they intend to test it in the general population.

"I think if things go well, we foresee that probably in the next two to four years, this test should be on the marketplace to be used for early detection of pancreatic cancer worldwide," Goel said.

Meanwhile, Grady's team is planning to investigate whether Shield helps get more people screened for colon cancer who are often missed, such as underrepresented minority groups or those who live in areas with restricted health care access.

Shield is "the first of, I think, a whole series of tests that we're going to be seeing coming up for screening for not only colon cancer but also for breast cancer, lung cancer, liver cancer," Grady said.

Four years later, tests show Gormly is cancer-free. He hopes his experiences help others who may be tempted to skip colon cancer screening.

"I hope that as a result of this [speaking up]," he said, "someone else tries it and has the same success I did."

Editor's note: This article was first published March 21, 2025 and republished Oct. 17, 2025

When the first cells appeared on Earth approximately 3.8 billion years ago, viruses were already here to greet them. Ever since, viruses have been devising ways to infect cells, and cells have been responding by evolving ways to stop these infections. This evolutionary dance eventually led to the development of your immune system.

A key aspect of your immune system is to distinguish "self" from "nonself" so it can destroy and remove foreign materials from your body. While this immune reaction protects you from viruses, it also has implications for how well foreign materials such as medications work.

I am a researcher studying ways to make drugs work better, including how to get them to the site of disease within the body before being removed or destroyed. One way to do this is to encapsulate drugs in nanoparticles — materials small enough to be taken up by cells. While these materials still trigger an immune response to get them out of the body, scientists like me have found that this reaction could actually be used to improve the effectiveness of cancer treatment.

The immune system and drug delivery

In addition to detecting pathogens, your immune system also responds to tissue damage. You might observe this reaction as inflammation — such as redness and swelling — when drugs are injected into your body with a needle.

Typically this inflammatory response is minimal. But the potential for a sustained reaction increases when drugs are administered slowly over a prolonged period of time, such as during chemotherapy infusions that can take an hour or more. For this reason, some patients are given anti-inflammatory medications before infusion to reduce the potential for an adverse immune response during treatment.

The most recent breakthroughs in getting drugs into the body is using nanoparticles. These materials — which can be made from lipids, proteins, gold or other components — have the advantage of being very small: The diameter of a typical nanoparticle is about 10-thousandths of a millimeter. Their small size allows diseased cells to easily take them up. So when nanoparticles contain drugs, they can act as a drug delivery system.

Despite being so small, nanoparticles can hold a large number of drug molecules, allowing them to deliver a potent cargo of treatment directly into a cell. They can also deliver drugs made of DNA and RNA. The most well-known example of this technology is the COVID-19 vaccine, which uses nanoparticles made of modified fat molecules to deliver mRNA that teaches the immune system to protect itself against COVID-19 infection.

Your innate immune system also identifies nanoparticles as foreign invaders when they are injected into your body. As a result, some patients experience an initial inflammatory reaction when the body tries to attack the nanoparticle.

But what if this reaction could actually be used to improve treatment?

Exploiting the innate immune response

For the past 30 years, my laboratory at the University of Colorado has been studying how nanoparticles deliver drugs. More recently, we have focused on understanding how the innate immune system responds to an injection of nanoparticles. While this immune reaction is typically considered a drawback, we wanted to explore whether it could enhance therapy.

In a 2022 study on how nanoparticles affect the immune response in mice, we found that the innate immune response triggered by an initial dose of nanoparticles carrying a drug will also reduce the effects of a second dose if it is injected shortly afterward — typically within days. It does this by clearing the drug out from the body more quickly. This reaction is similar to how an initial viral infection would trigger a short-term protective response against a subsequent infection from another virus.

One critical aspect of this protective effect involves the production of a protein called interferon lambda. This molecule "interferes" with the infection process by restricting viruses from gaining access to different tissues in the body. Researchers have previously tested this protein as a potential antiviral drug to treat COVID-19.

Similarly, the interferon lambda made in response to the first dose of nanoparticles limits the ability of the second dose to deliver the drug to healthy tissues in the body. However, it did not affect the nanoparticle's ability to access tumors, possibly because tumors can impair the immune response.

In conventional cancer treatment, chemotherapy drugs are used to kill the tumor. Because these drugs are also toxic to healthy cells, patients often experience side effects such as hair loss, gastrointestinal problems and skin rashes. Using nanoparticles to deliver cancer treatment could help reduce these side effects, and combining them with interferon lambda could allow the nanoparticle-encapsulated drug to stay in the body long enough to have its full effects.

Our team is studying whether directly injecting interferon lambda before chemotherapy with nanoparticles could help limit the amount of drug that ends up in healthy tissues while increasing their concentration in tumors. In an initial test of this strategy in mice with colon cancer, all mice that received interferon lambda saw increased survival time and reduced weight loss. A better understanding of how this effect happens could help researchers eventually test this approach to cancer treatment in human patients.

Scientists have a long way to go in developing nanoparticles that are as efficient as viruses at getting into cells. But our hope is that exploiting an immune response that evolved approximately a billion years ago to prevent viral infections could help reduce the toxic side effects from treatment while improving its effectiveness.

This edited article is republished from The Conversation under a Creative Commons license. Read the original article.

Human papillomavirus (HPV) vaccines can dramatically reduce the rate of infections that cause cervical cancer, even in people who haven't been vaccinated, a new long-term study reveals.

Most cases of cervical cancer are caused by high-risk HPV viruses, which can drive changes in cells that turn them cancerous. Two types of high-risk HPV are most likely to cause cervical cancer. After the introduction of HPV vaccines in the U.S., the shots reduced the amount of people testing positive for those cervical-cancer-causing viruses by a whopping 98.4% in vaccinated teens and young women in Cincinnati, the focus of the new study. Meanwhile, in unvaccinated people of the same age, the rates of infection still fell by 71.6% in the same time period.

This demonstrates that HPV vaccines, introduced in the U.S. in 2006, can lead to herd immunity, which is when a population becomes so resistant to the spread of a virus that even unvaccinated people are indirectly protected.

HPV is the most common sexually transmitted infection worldwide; that stat includes both low- and high-risk strains. While it's primarily known for its potential to cause cervical cancer, exposure to high-risk HPV can also lead to other cancers in both sexes, according to a statement released by the researchers. These include those affecting the anus, head and neck.

Scientists have known for many years that HPV vaccines are highly effective, significantly reducing the rate of cervical precancers in young U.S. women and preventing cervical cancer deaths. However, the new 17-year study, published Monday (Sept. 29) in the journal JAMA Pediatrics, found that the vaccines have also reduced high-risk cervical infections in adolescent girls and young women at increased risk of HPV, even when they themselves were not vaccinated.

Nearly all sexually active people get HPV at some point in their lives. The infections are typically symptomless and tend to go away on their own within two years. However, in some cases, they can persist and ultimately cause cancers.

A 2020 study published in The Lancet Global Health estimated that in 2018, there were 690,000 cases of cancer attributed to HPV worldwide, including 620,000 in women and 70,000 in men. Cervical cancer accounted for about 80% of these cancer cases. So while most people don't get cancer as a result of an HPV infection, the virus' prevalence makes it a major public health problem.

In the new study, the researchers analyzed data from six surveillance studies in Cincinnati, collected from 2006 — the year before the vaccine became available there — to 2023. The study included 2,335 adolescent girls and young women between 13 and 26 years old. They focused primarily on participants who had an increased risk for HPV because they had multiple sexual partners or a history of sexually transmitted infection.

Multiple HPV vaccines have been introduced since 2006, and this study assessed the effectiveness of three versions: the 2-valent version, which guards against HPV 16 and HPV 18, the HPV responsible for more than 70% of cervical cancers; the 4-valent version, which additionally covers HPV 6 and HPV 11; and the 9-valent versions, which protect against another five types.

During the study period, the rate of HPV infections fell as the vaccines became available and the proportion of vaccinated participants increased, from 0% to 82%. Infections covered by the 2-valent vaccine dropped by 98.4% among vaccinated individuals, while the remaining HPV types covered by the 4-valent and 9-valent vaccines dropped by 94.2% and 75.7%, respectively.

The 9-valent vaccine was just as protective as the 2-valent and 4-valent vaccines in clinical trials, lead study author Dr. Jessica Kahn, a professor of pediatrics at the Albert Einstein College of Medicine in New York, told Live Science. But the decline in virus types targeted by the 9-valent vaccine was lower in this real-world scenario because it was licensed more recently, meaning fewer participants had received at least one dose of that version by the time of the study.

Among unvaccinated participants, HPV 16 and HPV 18 infections dropped by 71.6% in the study population, while the remaining two strains covered by the 4-valent vaccine dropped by 75.8%, indicating a high degree of herd immunity. The researchers didn't have enough data to effectively look at all the strains covered by the newer 9-valent vaccine in unvaccinated people.

The findings are good news for highly vaccinated areas, but rates of cervical cancer are higher in poorer countries than in the U.S. Globally, only 31% of adolescent girls and 8% of adolescent boys between 9 and 14 years old have received one dose of an HPV vaccine, according to 2024 World Health Organization data, the latest available. Increasing vaccine uptake worldwide could have dramatic impacts.

"By expanding uptake of this highly safe and effective vaccine, and ensuring access to screening and treatment, we can achieve one of the greatest public health victories of our time: the elimination of cervical cancer worldwide," Kahn said.

This article is for informational purposes only and is not meant to offer medical advice.

A dietary change may make the fatal brain cancer glioblastoma more vulnerable to cancer therapies, a new study suggests.

The researchers behind the work think this dietary change exploits a key metabolic vulnerability in the cancer, and their work demonstrates that the approach extends survival in mice when used in combination with chemoradiation therapy.

The study, published Sept. 3 in the journal Nature, suggests that a deeper understanding of how tumor cells tweak their metabolisms in the pursuit of all-out growth could open treatment windows for this notoriously deadly cancer.

Healthy cells in the brain need fuel to maintain their extensive list of functions, like electrical signaling and the release of chemical messengers. Cancer cells dispose of these normal processes as they rewire to become "professional dividing cells," said study co-author Costas Lyssiotis, a professor of oncology at the University of Michigan.

These changes are of great interest to cancer researchers because they may allow therapies to distinguish between healthy cells and tumors, making them more targeted.

"The real art of delivering therapy is making it so that you kill the cancer way more than you kill the normal [cells]," Lyssiotis told Live Science.

Related: New treatment for most aggressive brain cancer may help patients live longer

The work, coordinated by University of Michigan oncologist Dr. Dan Wahl, assessed how glioblastoma warps its metabolism in both human and animal brains. The study ambitiously combined laboratory research and clinical practice by drawing some of its data from tissue taken from the brains of patients undergoing cancer surgery. The study required the collaboration of experts in human and rodent brain surgery, metabolic pathways, and molecular analysis.

The protocol began in the hours before surgery. The patients received an infusion of glucose, which was tagged so that it was detectable by molecular analysis techniques. The glucose flowed through their bloodstreams and into both their healthy and tumorous cells.

A common approach for glioblastoma surgery is to remove the tumor and some surrounding brain tissue to minimize the risk of the cancer quickly growing back. The team took blood samples every 30 minutes during surgery and then flash-froze the excised tumor and healthy tissue for analysis.

These extracted cells had metabolized the glucose, and the researchers tracked the molecules' path through the cells. In concert with experiments in mice, the researchers gained a clear view into what tumor cells were doing differently as they gobbled up the sugar.

Healthy cells metabolized glucose for cell processes like respiration, in which sugar and oxygen are converted into fuel for the cell. These cells also converted glucose into an amino acid called serine, a key ingredient for important neurotransmitter molecules.

The tumor cells, by contrast, set these processes aside. Instead, the cancer cells directed glucose to produce nucleotides — the building blocks of DNA. These molecules are vital fuel sources for the tumor cells' endless replication.

Chemoradiation therapies attack cancer by destroying its DNA, but this rerouting gives the cancer cells a steady source of nucleotides with which to repair the damage. The study showed that the tumor cells also scavenged serine from surrounding tissues to further fuel their growth.

Here, Wahl and his team saw an opportunity. They put mice that had been transplanted with human cancer cells on a feeding regimen that drastically reduced their dietary serine. Lyssiotis suggested that this could potentially be replicated in human cancer patients with a low-protein diet supplemented with serine-free protein shakes.

As this cut the amount of serine available for tumor cells, it forced the cancer to reroute its glucose metabolism back into serine production. In turn, this slashed their nucleotide synthesis and made the cells more vulnerable to chemoradiation. Mice given this treatment combination lived longer than mice that were only given chemoradiation.

Lyssiotis explained that this vulnerability would likely work for a limited time, as glioblastoma cells can deftly adapt their metabolisms. In addition, some tumor cells appeared to rely less than others on scavenged serine. "If you can hit that sweet spot, you deprive them of serine, and you come in with the therapies, you get them before they figure out a workaround," he suggested.

Wahl is already beginning work on a follow-up clinical study to back up these results in mice with data from human cancer patients.

"We hope to be bringing that to our patients later this year or early next year," he said. That work will also involve challenges and coordination. "Going through cancer treatment is hard. We're asking people to come up for radiation every day, to take chemotherapy. I think asking someone to also follow a prescribed diet could be tricky," he added.

But the current study has provided valuable information that will inform that future clinical work. "Part of what we're excited about is that this isotope tracing protocol [tracking the tagged glucose] can tell us which tumors are making serine from glucose and which tumors are taking serine up from the environment," Wahl said.

Lyssiotis noted that the paper's pioneering metabolic analysis has identified additional dietary changes that could be explored in future work. Serine modification is the easiest to implement, for the moment. "We think that that's just the tip of the iceberg," he said.

This article is for informational purposes only and is not meant to offer medical or dietary advice.

"Getting your tubes tied" is a colloquial way to say that someone is undergoing tubal ligation, a sterilizing surgical procedure that involves closing off the fallopian tubes.

In non-medically assisted pregnancy, an egg travels from the ovary to the uterus via the fallopian tubes, also called uterine tubes. Tubal ligation prevents this movement by permanently blocking, clipping or removing the tubes, thus keeping the egg from becoming fertilized. The removal of the tubes, called a salpingectomy, is a type of tubal ligation.

The procedure is extremely effective, with a 99% free-from-pregnancy rate. That number rises to 100% for surgeries that use large incisions to access the tubes, rather than minimally invasive medical tools that can navigate the body through small incisions.

"It's a great option for family planning that does, unfortunately, involve a surgical procedure," Dr. Andrew Rubenstein, director of General Obstetrics and Gynecology at NYU Langone Health, told Live Science.

Side effects are minimal, but can include shoulder pain, bloating, abdominal cramping, nausea and dizziness, according to Cleveland Clinic. The shoulder pain is related to gas used to temporarily inflate the abdomen during some tubal ligation procedures; that gas can linger and irritate the neck, shoulders and chest for up to a couple days after surgery.

Tubal ligation can be performed whether or not the patient has had a pregnancy previously, Rubenstein explained.

Related: Tube-tying surgeries and vasectomies skyrocketed post-Roe

Regardless of when a person gets their tubes tied, extensive consultation between the patient and the physician is required beforehand. The patient's partner may also be included in the consultation, if applicable.

"It is shared decision making amongst the team members," Rubenstein said, describing the process of deciding what form of birth control is the best approach for each individual patient. "It's not a single episode event and then surgery is scheduled. It does require some doctor-patient relationship."

How does the surgery work?

There are four main methods for completing a tubal ligation, each using a different technique to block the travel of an egg. Doctors may remove both tubes completely — which is called a bilateral salpingectomy, or "bisalp" for short — or partition the tubes by cauterizing, clipping or folding them.

(Unilateral salpingectomies, which remove only one tube, are not a sterilizing procedure but can be used to treat conditions like ectopic pregnancy.)

The method a physician chooses, and whether they agree to carry out the procedure at all, in part depends on a patient's clinical history, Rubenstein said. Doctors will consider factors like age, past surgical procedures and body mass index to see what's feasible for a given patient.

The procedure is often completed through two small incisions, one just below the navel and the other on the lower abdomen above the pelvis. Using laparoscopic tools — a small camera and accompanying instruments that allow the surgeon to see within the body — the physician can complete the permanent operation.

Sometimes a tubal ligation is performed as a preventative treatment to decrease a patient's chances of contracting ovarian cancer. Evidence suggests that ovarian cancers often arise in the fallopian tubes, and that removing the tubes can cut the risk.

"It doesn't eliminate it, but it definitely reduces that risk for patients," Rubenstein said. It's currently unclear by how much tubal ligation lowers the odds of developing ovarian cancer, but some research suggests it decreases by 24% to 42%.

Anyone with fallopian tubes who is uninterested in getting pregnant in the future and already plans to undergo pelvic surgery should consider taking this preventative measure simultaneously, the Ovarian Cancer Research Alliance and the Society of Gynecologic Oncology suggest.

Rubenstein warned that not all operating rooms will perform tubal ligations. "Certain organizations will not allow you to do tubal ligation in their facilities based on religious beliefs, so they have to be done then in a nondenominational facility," he said.

Is it permanent?

Like any operation, tubal ligation can fail — in this context, failure means the patient becomes pregnant after the surgery.

"It's extremely rare," Rubenstein said, but it can happen and is more likely to occur for younger patients. Within the first year after the procedure, the failure rate is estimated to be 0.1 to 0.8% across all patients.

Some providers won't perform the procedure on someone younger than 30, Rubenstein said, on the basis that the patient might later come to regret it. One 2022 study that surveyed about 1,500 patients found that 12.6% of people who underwent sterilization at ages 21 to 30 and 6.7% of those who underwent sterilization when they were older than 30 regretted their choice. Notably, the majority of the patients — 92% — were in the over-30 group, so the sample of under-30s was somewhat small.

To place the 2022 study in greater context, the average regret rate reported is similar to that for knee replacement surgery, at around 10%.

Rubenstein thinks it is important to emphasize that tubal ligation is a permanent surgery. "People have a misconception that tying your tubes is similar to tying your shoelaces. You can tie and untie them," he said.

While it is medically possible to reverse the operation when the tubes have not been fully removed, just cauterized, clipped or folded, most doctors won't do so, Rubenstein said. When they are done, reversal surgeries enable about 73% of patients to get pregnant and 53% to give birth, a review of 135 cases found.

In contrast, Rubenstein described in vitro fertilization (IVF) success rates in such situations as "exceptional." In other words, "we would recommend to that patient to have an IVF cycle and then a transfer of that embryo into the uterus rather than trying to reconnect the tubes." IVF never requires an egg to travel through the tubes, so the procedure would still work for a person lacking tubes.

This article is for informational purposes only and is not meant to offer medical advice.

Cannabis smoke can seem gentler than tobacco's, but that impression of marijuana may be deceptive. Deep in the lungs, the drug's chemistry is far from benign, recent research suggests. Some studies have even linked heavy cannabis use to a heightened risk of some cancers, including those of the head and neck.

So is there a clear link between cannabis and cancer, and if so, what causes it?

Each lungful of cannabis smoke is a brew of the high-inducing ingredient tetrahydrocannabinol (THC), fine particulates, and certain carcinogens that are also found in tobacco. But cannabinoids may bring their own twist by quietly rewiring the lungs' immune settings.

"The airway's protective lining weakens, antiviral signals falter, and inflammation flares," said Raphael Cuomo, a scientist working at the intersection of cancer prevention and addiction at the University of California, San Diego. In one study with mice, cannabis smoke dulled both tumor-fighting and infection defenses. In another, THC blunted the effects of immunotherapy, weakening tumor-killing immune cells in the body.

Cannabis also triggers other changes in the immune system, according to studies in humans, cells and lab mice. In the airways, levels of proteins tied to inflammation spike when cannabis is used consistently. A protein called MUC5AC, which lines and protects the respiratory tract, is made in excess in certain cells, hinting at early tissue changes. Cannabis smoke can skew the enzymes that maintain tissue and switch off genes that respond to toxins.

The responses of the lungs' patrol cells — alveolar macrophages — can be stunted. And in the blood, shifts in cellular messengers called cytokines and faint changes in epigenetics become a molecular diary of exposure.

Related: Could cannabis treat cancer someday? Here's what the science says so far

In summary, "cannabis smoke, from its toxic byproducts to THC, can irritate lungs and weaken immunity," Sayantan Bhattacharyya, a cancer systems biologist who will soon be a senior postdoctoral scientist at the University of Limerick in Ireland, told Live Science.

But immune disruption is only one factor that might raise cancer risk. Cannabis smoke may also tug on deeper levers inside cells — the molecular switches that cancers use to grow and spread.

Among these, few are as infamous as the epidermal growth factor receptor, or EGFR. In one of the few studies of its kind, Bhattacharyya examined 83 men with glottic cancer, which affects the voice box, and found that cannabis smokers in the group had markedly higher activation of EGFR and related cancer proteins than either tobacco smokers or nonsmokers.

"EGFR governs [cell] growth, repair, and survival," Bhattacharyya said. "In cannabis smokers, constant activation can fuel unchecked proliferation, speed genetic damage, and hasten the leap toward cancer — triggering earlier onset, faster spread, and treatment resistance." That said, Bhattacharyya's study included only 83 people with one type of cancer, so more work is needed to know if the results are broadly applicable.

Bhattacharyya sees two priorities for future research. One is to develop realistic lab models — such as "organoids," 3D-printed tumors and organ chips — to study how cannabis amplifies EGFR. The other is to probe potentially dangerous additives that might be lurking in unregulated cannabis products, he said.

For all the unsettling biology uncovered in laboratory studies, real-world studies of cannabis smokers tell a mixed story. Some research links heavy cannabis use to higher cancer risk, while others find no clear connection. Still, Cuomo maintains that long-term use of the drug may increase the odds of developing cancer, based on what we know so far.

For people who already have cancer, however, Cuomo has shown that cannabis use isn't linked to an earlier death — a puzzle researchers now call "Cuomo's paradox." In fact, studies have found that, in cancer patients, cannabis can boost appetite and curb chemotherapy-induced nausea, even as its smoke may potentially be planting the chemical and cellular seeds of disease.

The challenge going forward will be to accurately assess both the benefits and harms of cannabis in order to weigh them against one another.

Editor's note: This story was updated on Aug. 21, 2025, to note that Bhattacharyya will hold a position at University of Limerick.

This article is for informational purposes only and is not meant to offer medical advice.

A universal cancer vaccine in development could help rev up the immune system against tumors and supercharge the effects of existing cancer therapies, an animal study suggests.

Similar to vaccines for viral infections like the flu, many cancer vaccines are designed to help the immune system recognize specific proteins. However, while conventional vaccines aim to prevent disease, cancer vaccines are currently being developed to clear away cancers already growing in the body and to help prevent treated cancers from coming back.

Nonetheless, conventional vaccines and cancer vaccines often work similarly. The flu shot trains the immune system to look for unique proteins found on the surface of influenza viruses, while cancer vaccines typically teach immune cells to spot unique features of cancer cells.

But there's a challenge: These cancer proteins of interest can often be unique to individual patients, meaning each cancer vaccine may need to be specially formulated for each patient. Although it's possible to craft such personalized vaccines, they take time to make — and, in the interim, the patient's cancer mutates, potentially causing the vaccine to be less effective.

"It can be months from the time you get a patient's specimen to when they actually have a personalized therapy," said study senior author Dr. Elias Sayour, a pediatric oncologist at University of Florida Health. Sayour and colleagues wondered if they could design a cancer vaccine that would not require this personalization and instead ignite a general immune response to keep cancer at bay.

"The idea that something could be available immediately, albeit in a nonspecific way … could be revolutionary for how we bridge therapy and how we manage patients," Sayour told Live Science.

Related: New mRNA vaccine for deadly brain cancer triggers a strong immune response

An "off-the-shelf" cancer vaccine

The experimental vaccine, described in a report published July 18 in the journal Nature Biomedical Engineering, is built upon messenger RNA (mRNA), which also formed the basis of the first COVID-19 vaccines that continue to be updated now.

mRNA acts as blueprints that cells then base new proteins on. In the COVID-19 vaccines, the molecule contains instructions for a bit of the coronavirus; in the new cancer vaccine, it carries instructions for a substance that raises the body's first-line immune defenses, poking the "innate" immune system rather than the "adaptive.".

In particular, the vaccine aims to boost the body's production of type-I interferons — immune messengers that play important roles in controlling inflammation and spotting cancerous tumors in order to eliminate them. In a series of experiments in lab mice, the researchers demonstrated that this signaling is key to snuffing out tumors early in their development. The signals help rally the immune system to attack the tumors and hinder the cancer's growth, and if you block them, tumor growth goes haywire.

Additionally, these experiments showed that this early interferon activity is vital to a common form of cancer treatment, called immune checkpoint inhibitors. These treatments rip the breaks off of immune cells so they maintain a high level of activity and kill off cancer efficiently.

Cancer has ways of hijacking interferon signals and thus thwarting the anti-cancer immune response that follows — so the cancer vaccine acts as a kind of immune "reset," Sayour explained.

The researchers used the vaccine in combination with a checkpoint inhibitor in a mouse model of melanoma, a type of skin cancer. In mice with treatment-resistant tumors, the combo of treatments worked better than checkpoint inhibitors alone, the team found. They also tested the vaccine on its own in mouse models of other cancers, including glioma (a brain cancer) and pulmonary osteosarcoma (bone cancer that's spread to the lungs). It showed promising anti-cancer effects when applied by itself, as well.

For this early work, the team tested a few different mRNA formulations to stir up the interferon response and found that each did so effectively. More work is needed to understand if the mRNA molecules themselves or the proteins they're used to make are more important for triggering this generalized response, Sayour noted.

The current study focused on solid tumors, which tend to be more resistant to immunotherapy than blood cancers are, Sayour said. But "I personally think this can be used for all forms of cancer," he added. "I believe this is a universal paradigm that can be used to treat cancer." In particular, he could see it being applied as secondary prevention, to help stop treated cancers from coming back.

"This exciting and novel paper shows promising evidence that giving the immune system a short, targeted boost at just the right time can help previously unresponsive tumors respond to immunotherapy," said Diana Azzam, an associate professor and scientific director at the Center for Advancing Personalized Cancer Treatments at Florida International University.

"This approach could be especially helpful for 'cold' tumors — types of cancer that usually don't trigger a strong immune response, like pancreatic, ovarian, and some types of breast cancer," Azzam, who was not involved in the study, told Live Science in an email. These tumors hide from the immune system and can be difficult to target with immunotherapy, so it's possible that this type of vaccine could help expose these cancers to attack.

"While more research is needed to confirm how well this approach will work in people, the encouraging results in mice offer a strong foundation," Azzam said. In people, you'd want to ensure that the vaccine mounts a helpful immune response without sparking unwanted inflammation in the long run, for instance. "Future studies will address key questions around safety, consistency, and long-term effectiveness in real-world cancer patients," she concluded.

Meanwhile, Sayour and his colleagues have launched a human trial testing a two-hit approach: an off-the-shelf cancer vaccine followed by a personalized one. They're working with patients with two types of recurrent cancers: either pediatric high-grade glioma or osteosarcoma.

"This approach saves valuable time needed for personalized vaccinations and may induce rapid immunity that can be further seized upon by personalized therapy," Sayour said.

This article is for informational purposes only and is not meant to offer medical advice.

Children born by planned cesarean section are 21% more likely to develop acute lymphoblastic leukemia (ALL), a childhood cancer, than those born vaginally, a new study finds.

The research, conducted in Sweden, is consistent with previous studies that also found a link between pediatric ALL risk and C-sections. More recent research, including this latest study, has specifically connected the majority of that risk to planned C-sections. In this study, planned C-sections were defined as those initiated prior to labor.

But crucially, the risk of ALL, and childhood cancer in general, remains low across the board, said Joseph Wiemels, a professor of population and public health sciences at the University of Southern California who was not involved in the work. In the U.S., about 4.8 in 100,000 children are diagnosed with leukemia per year. So while "the relative risk [for ALL] is significantly higher" for babies born by planned cesarean, Wiemels cautioned that that the risk is "still relatively low" overall.

Cesarean section "is a vital and often life-saving component of modern obstetric care," lead study author Christina Evmorfia-Kampitsi, a postdoctoral researcher at Karolina Institutet, told Live Science in an email. Some people give birth by planned C-section due to maternal conditions, such as preeclampsia, or to protect the baby's health because they aren't getting enough oxygen, for example.

"Our findings should not be a cause for concern when the procedure is medically indicated," Evmorfia-Kampitsi said.

Related: Babies' brain activity changes dramatically before and after birth, groundbreaking study finds

Confirming a known link

What's unique about the study, published July 4 in the International Journal of Cancer, is that researchers controlled for a range of characteristics in mothers and newborns and still found a higher risk of ALL in children born by planned cesarean.

"Thanks to the richness of Swedish register data, we were able to adjust for a wide range of maternal, pregnancy, and neonatal [newborn] factors," Evmorfia-Kampitsi said. "This helps strengthen the evidence that the association is not merely due to underlying conditions that might have led to the CS [C-section] in the first place."

Controlling for these other factors is important, Wiemels said, in part because maternal ages above 35 are also associated with a higher risk of children developing ALL. There's also a link between birth defects and ALL risk, as well as environmental factors like radiation. But because ALL occurs at such young ages, researchers have been exploring factors before and just after birth that may lead to its development, Dr. Danielle Daee, program director of the genomic epidemiology branch at the National Cancer Institute who wasn't involved in the work, told Live Science in an email.

For the study, researchers looked at the mode of delivery — vaginal, planned cesarean or unplanned cesarean — in more than 2.4 million births that took place in Sweden over 20 years. Data on newborns' weights, birth defects, and whether their mothers were overweight or had obesity, diabetes or preeclampsia were also examined. Additionally, they looked at the incidence of ALL among these children over time.

The researchers also grouped the kids based on the decade in which they were born, to account for changes in obstetric practice, the rate of C-sections, changes in how childhood cancers are diagnosed, and other factors that might vary over time, Evmorfia-Kampitsi said.

More than 375,000 of the children, about 15%, were born by C-section, including about 213,000 planned, which were initiated prior to labor starting. About 1,200 of the 2.4 million children, or 0.05%, developed ALL.

The risk of ALL was higher among the babies born by any type of C-section than among those born vaginally. There was a slight increase in risk tied to unplanned C-sections, which began post-labor, but the risk was highest among those born by planned cesarean, initiated before labor began.

The planned C-sections could be further divided into "planned" and "acute," with the latter meaning there was some sort of immediate medical need, like fetal distress. These acute cases didn't seem tied to any increase in cancer risk — but because there were only a handful of such cases, it's difficult to draw firm conclusions.

“These results should be interpreted with caution," Evmorfia-Kampitsi said. "Our primary finding remains the increased risk associated with planned pre-labor CS."

Related: Scientists reveal surprising factor that may prolong pregnancy

Cause for concern?

Childhood ALL is most often diagnosed in children under 5 years old, and the study findings were only statistically significant for the children in this age group. In other words, the connection between planned C-sections and ALL seems clearest in that age range, Evmorfia-Kampitsi said.

The study may "tell us something about leukemia risk, and the mechanisms behind that risk," Wiemels suggested.

On that front, it's known that there are genetic mutations that can develop before birth and cause children to be born with pre-leukemia cells. However, more children are born with these cells than actually develop full-blown cancer, said Erin Marcotte, an associate professor in the Division of Pediatric Epidemiology & Clinical Research at the University of Minnesota, who wasn't involved in the new study.

"It's likely that most children are able to cull those cells," Marcotte told Live Science in an email. But how?

There are two leading theories as to how this works, and how those mechanisms may be compromised by planned C-sections. The first suggests that babies born via C-section miss out on exposure to microbes in the vaginal canal, which may promote a more "permissive" environment for leukemia to develop, Wiemels said. Babies born via C-sections that begin before labor are exposed to fewer microbes than those whose C-section start after labor because, at that point, the water has broken.

The second hypothesis is that babies born by planned C-section miss out on short-term exposure to stress hormones that they would typically encounter during labor. It's thought that these hormones may help eliminate pre-leukemia cells.

Adding to the idea is the fact that corticosteroids are a mainstay of childhood leukemia treatments, and are similar to body-made cortisol. Additionally, Kjeld Schmiegelow, a clinical professor at the University of Copenhagen, has hypothesized that the stress that stems from infections in early childhood can help eliminate pre-leukemic cells.

Whatever the root cause of the link, the absolute risk of ALL remains low even in the context of C-sections. But it's potentially something for doctors to consider, Evmorfia-Kampitsi said. "When a CS is being considered without a clear medical indication, it's important to be aware of potential long-term outcomes," she said.

Still, more research on the relationship between ALL and planned cesarean is needed, as countries with higher rates of cesarean deliveries don't always have higher rates of ALL. Since the study was done in Sweden, "it is plausible, but not confirmed, that other populations, with different demographic features and environmental exposures, may have a similar result," said Daee.

This article is for informational purposes only and is not meant to offer medical advice.

Why is heart cancer so rare? – Jackson, age 12, Davis, California

You probably know someone who is affected by cancer. This disease results when cells divide uncontrollably and can make a person sick, sometimes very seriously.

Cancer can occur anywhere in the body because every tissue and organ is made up of billions or even trillions of cells. But there are some parts of the body where cancer doesn't happen as often, such as the heart. Studies show 3 in 10,000 people develop heart cancer. In comparison, 1 in 20 women are expected to develop breast cancer. Why is that?

I'm a biologist who specializes in the blood vessels of the cardiovascular system. A big part of my work focuses on how cells interact with their environment to regulate the function of tissues and organs. Disease can develop when things go wrong.

Turns out, heart cells have unique features that make them super resistant to cancer.

How cancer starts

Cells produce more cells to grow, replace older or worn-out cells or to repair damaged tissues. This process is called cell division. Each type of cell in the body divides at different rates based on multiple factors, including what their function is and a person's age.

For example, the cells of a growing human embryo divide extremely fast, undergoing four divisions in three days. The cells that make up the skin, nails and hair regularly replenish across your lifespan. Bone cells divide at a rate that will give you an entirely new skeleton approximately every 10 years.

Whether and how often a cell divides is tightly regulated by a series of molecular checkpoints. During cell division, genes within DNA are duplicated and evenly distributed into two daughter cells. Damage to these genes caused by exposure to harmful chemicals, ultraviolet light or radiation can result in mutations that cause disease. Mutations can just happen randomly, too. When there are mutations on the genes regulating cell division, cancer can develop.

Related: The 10 deadliest cancers, and why there's no cure

What protects heart cells from cancer?

Even though the heart is the first organ to form and start working during early development, cells in the adult heart divide very few times after birth, with division dramatically declining after age 20. In fact, less than 50% of heart cells are replaced over the course of an average human life. That means half of the heart cells you're born with will be helping pump blood for your entire life.

This low rate of cell division in the adult heart likely serves as its primary defense against cancer. The less often a cell divides, the fewer opportunities there are for mistakes during DNA replication.

The heart is also less directly exposed to cancer-causing factors, such as UV light on the skin or inhaled substances in the lung, due to its protected location in the chest.

Unfortunately, the heart's low rate of cell division has some downsides, such as a reduced ability to repair and replace cells damaged by disease, injury or aging.

Why heart cancer still happens

Even with the heart's resistance to cancer, tumors may still form.

When cancer is found in the heart, it's often the result of cancer cells migrating from another part of the body to the heart. This process is called metastasis. Certain types of skin cancers or cancers in the chest are more likely to spread to the heart, though this is still rare.

When they do happen, heart tumors can be quite serious and more aggressive than other cancers. A study analyzing more than 100,000 heart cancer cases in the United States found that patients who underwent surgery and chemotherapy to treat their heart cancer survived longer than those who did not.

Successful cancer care spans multiple areas of medicine. These include palliative care, which focuses on relieving pain and addressing symptoms, and integrative medicine, which considers the mind-body-spirit connection.

Heart cancer holds clues to heart regeneration

Understanding how heart cells divide and what causes that process to change offers clues about disease and shapes ideas for new treatments.

For example, research into how heart cells divide helps scientists better understand why the heart doesn't heal well after a heart attack. Researchers found that although failing hearts have more dividing cells than healthy hearts, they need help to recover fully.

New technologies, such as the ability to reprogram blood cells into heart cells, have allowed researchers to develop new heart disease models to study and one day achieve heart regeneration. This opens doors for new treatments for heart diseases, including cancer.

Understanding why cancer doesn't happen is just as important for developing new and better treatments as knowing why it does. The answers to both questions lie truly at the heart.

Hello, curious kids! Do you have a question you'd like an expert to answer? Ask an adult to send your question to CuriousKidsUS@theconversation.com. Please tell us your name, age and the city where you live.

And since curiosity has no age limit — adults, let us know what you're wondering, too. We won't be able to answer every question, but we will do our best.

This edited article is republished from The Conversation under a Creative Commons license. Read the original article.

Scientists are developing a test that uses a tiny blood sample to detect pancreatic cancer in its early stages.

If caught early, pancreatic cancer can potentially be treated. However, patients usually aren't diagnosed until the cancer has already spread, slashing their chances of survival. The disease is predicted to cause more than 51,000 deaths in the U.S. this year, accounting for over 8% of the nation's total cancer deaths.

One reason pancreatic cancer is often diagnosed at an advanced stage is that doctors have no routine screening tests for the disease, although some tests are being explored for people known to be at high risk. Now, researchers are developing a test that they hope could diagnose the deadly cancer with just one drop of blood.

They call the test PAC-MANN, which stands for "protease activity-based assay using a magnetic nanosensor," and they described it in a paper published in the journal Science Translational Medicine earlier this year.

Although the test has shown some promising early results, an expert told Live Science it is not yet ready to be used as a screening tool.

How PAC-MANN works

Just as the classic arcade game hero Pac-Man chases and gobbles ghosts, pancreatic tumors send out protease enzymes that chew through surrounding tissue. Protease enzymes break down proteins, helping cancer cells enter the bloodstream and metastasize, or spread beyond their original location.

Related: Simple blood tests could be the future of cancer diagnosis

However, these enzymes appear in relatively low abundance in the bloodstream, and their activity levels vary among individuals with cancer. That makes their detection challenging with existing technologies.

To make these enzymes easier to detect, PAC-MANN uses tiny magnetic beads coated with fluorescent "probes." The idea is that, when a drop of blood from a cancer patient is added, tumor-made proteases slice the probes off the beads, releasing the fluorescent tags. A strong magnet pulls out all the beads, leaving only the freed fluorescent pieces.

The remaining glow, measured with a lab device called a fluorometer, is the readout. The more fluorescence, the higher the protease activity, signaling the likely presence of a tumor. The probes used in the test specifically react to MMP2, an enzyme identified as a standout in the blood of people with pancreatic cancer, compared to healthy individuals. That said, the enzyme is not unique to the cancer, as it has other known biological functions.

"The PAC-MANN assay requires such a minuscule volume of blood," study co-author Jared Fischer, a scientist with the Oregon Health & Science University (OHSU) Cancer Early Detection Advanced Research Center (CEDAR), told Live Science in an email.

So little blood is required that users could potentially use at-home skin prick or microneedle devices, "thus removing the need for a venous blood draw and a phlebotomist," as well as reducing the equipment and labor needed to run the test, he said.

Putting PAC-MANN to the test

The team validated the test using blood samples from 110 patients with pancreatic ductal adenocarcinoma (PDAC), the most common type of pancreatic cancer. They also examined blood from 170 healthy individuals, 45 people with pancreas inflammation (pancreatitis), and 31 with pancreatic neoplasia, meaning benign pancreatic tumors that can sometimes be precursors to cancer down the line.

They found that PAC-MANN correctly detected 73% of the PDAC cases. The detection of early-stage PDAC, specifically, was a little lower, at 62%. The test also correctly identified 98% of the noncancerous samples as such. That means, overall, 27% of the PDAC cases wrongfully came back "negative," and that 2% of the noncancerous samples were falsely identified as cancerous. These two key metrics are respectively known as test "sensitivity" and "specificity."

The team then tried combining PAC-MANN with a test for CA 19-9, another substance released by pancreatic tumors. High levels of CA 19-9 can be a sign of pancreatic cancer, but because other conditions can also drive up CA 19-9, they're not used for stand-alone cancer screening.

When PAC-MANN was combined with the CA 19-9 measurement, the combination test's sensitivity increased to 87%, on average, and it was 85% for early-stage cancer. The specificity fell slightly, though, to 96%.

The hope is that PAC-MANN could be used as a screening tool for people known to be at high risk for pancreatic cancer, study co-author Jose Montoya Mira, a research engineer at CEDAR, said in a statement. It could also be used alongside cancer treatments to see how well they're working, the authors said. CA 19-9 is an example of a test already used for this latter purpose.

However, Dr. John Neoptolemos, a research associate at the University of Heidelberg in Germany, urged caution. Protease enzymes are not unique to cancer, he told Live Science in an email. The enzymes play a variety of roles in the healthy body, such as aiding digestion and immunity.

"The strategy has a low probability of being used for early detection," Neoptolemos said. "The assay is not directly specific for cancer and has poor specificity for screening."

Neoptolemos added that there are now promising artificial-intelligence-based tests being developed for identifying and screening high-risk populations. As such, PAC-MANN would have to show clear added value over those emerging methods, Neoptolemos said.

All that said, PAC-MANN is still in development. Its makers are now expanding their studies, especially focusing on high-risk groups, to see if PAC-MANN can detect tumors earlier than currently possible. Montoya and Fischer have filed a patent application for PAC-MANN and are in the process of licensing the assay to a company.

This article is for informational purposes only and is not meant to offer medical advice.

A man developed painful swelling in his right middle finger and right big toe over the course of six weeks, causing the digits to take on a club-like shape. It turned out that the strange swelling was a rare sign of cancer that had spread through his body.

Prior to developing the swelling, the 55-year-old had been diagnosed with metastatic squamous-cell lung cancer, according to a report of the case published July 16 in The New England Journal of Medicine. This type of cancer starts in the flat, thin cells that line the airways, and in this case, the cancer had reached an advanced stage and spread, or metastasized, to other parts of the body.

After noting the swelling in his finger and toe, the man reported to the hospital for examination. Doctors found that the tip of each affected digit was red and swollen. They also noted that an ulcer was forming near the nail of the affected toe. The swollen areas were firm to the touch and tender, the doctors reported.

Scans of the man's affected hand and foot revealed "destructive lytic lesions that had completely replaced" the bones in the tips of the middle finger and big toe. Lytic lesions are areas where bone has been destroyed, leaving holes or blank spaces in the skeleton. Such lesions are typically driven by a disease process like cancer.

Cancer that has spread to finger or toe bones may mimic gout or osteomyelitis on a physical examination, but scans called radiographs can help to diagnose the condition, the patient's doctors noted. Gout is a form of inflammatory arthritis and osteomyelitis causes inflammation in bones, often due to infection, so both conditions can cause visible redness and swelling.

Based on his radiographs, the man was diagnosed with acrometastasis, a relatively rare form of cancer spread that occurs below the elbow or knee. Acrometastases account for only about 0.1% of cases in which cancer has spread to the bones, according to a 2021 review.

Related: New blood test detects cancers 3 years before typical diagnosis, study hints

Most often, this rare symptom is seen in patients who are already known to have cancer, as in the recent case. But sometimes, the symptoms of acrometastasis are the first sign of a previously undiagnosed cancer. It is most often associated with cancers of the lung, gastrointestinal tract and genitourinary tract, according to the review.

Acrometastases are seen much more often in males than in females, according to the review, which looked at about 250 cases of the conditions that had been published between 1986 and 2020. This sex difference has also been flagged in other reviews of the literature. The bones of the fingers and toes were more likely to be affected than the other bones in the hand and foot, the literature suggests.

Acrometastases are fairly rare because, when cancer spreads to bone, it's usually drawn to the bone marrow, which in adults is found primarily in the long bones of the arms and legs, ribs, backbone, breastbone and pelvis. By comparison, finger and toe bones contain much less marrow. They also receive less blood flow than bones located closer to the heart, so that also may help to explain why cancer spreads to the fingers and toes less frequently, the review suggests.

Because acrometastases are usually seen in late-stage cancer, they're associated with poor survival time — often less than six months from diagnosis of the condition. As such, treatments are typically focused on relieving the patient's pain and retaining as much functionality of the hand or foot as possible. In the 55-year-old's case, doctors started palliative radiotherapy, which aims to relieve a person's symptoms rather than cure their disease.

The doctors reported that the patient died three weeks later from complications of refractory hypercalcemia — dangerously high calcium levels in the blood that do not fall in response to standard treatments. This condition is often, but not always, tied to cancer.

This article is for informational purposes only and is not meant to offer medical advice.

Some chemotherapy drugs cause more damage to healthy cells than other chemo options do, a new study finds.

The researchers have found four new mutational signatures — patterns of DNA damage left by certain classes of drug — linked to chemotherapy. They also pinpointed some medications that can even "artificially age" healthy blood cells via these mutations.

The findings, published Tuesday (July 1) in the journal Nature Genetics, could help doctors select cancer treatments that cause minimal knock-on damage to patients' bodies while still attacking their cancer, the scientists say.

Some cancer chemotherapy medications destroy rapidly dividing cells by damaging their DNA, triggering cell death. While cancer cells fit that description, there are also healthy cells that divide quickly, such as those found in bone marrow and blood. This new study aimed to find out how chemo impacts those healthy cells and to do so in unprecedented detail.

The research team compared the blood of 23 people, ages 3 to 80, who were previously treated with chemotherapy with the blood of nine subjects without histories of cancer or chemo. Collectively, the people in the chemo group had received 21 different therapies, including platinum and alkylating agents, which kill cancer cells by damaging their DNA.

The team isolated blood stem cells and mature blood cells from the groups. They extracted DNA from the cells and put them through whole-genome sequencing. Using mathematical models, they pinpointed a number of mutational signatures in each cell's DNA, four of which had never before been reported to the COSMIC database of mutational signatures and are heavily suspected to be caused by chemo.

Related: Some early-onset cancers are on the rise. Why?

Although some of the signatures were present in samples from both the cancer-free and chemo-treated groups, 11 appeared only in the chemo group. That included the four new signatures.

But interestingly, not all medications within the chemo group caused the same degree of mutational burden. For example, the team found that cyclophosphamide, which is used to treat cancers such as multiple myeloma and breast cancer, causes far fewer mutations than others in its class.

More mutations mean a higher risk of getting another kind of cancer after treatment, called a secondary tumor. "The risk of secondary malignancy with cyclophosphamide is known to be lower" than with other drugs of its class, first study author Dr. Emily Mitchell, a hematologist and researcher at the Wellcome Sanger Institute and a clinician at Cambridge University Hospital, told Live Science in an email. That said, the risk is not zero.

Cancer is caused by mutations that lead to uncontrolled cell growth. But genetic mutations, in general, are also linked to aging.

"Each cell in our body accumulates mutations over time in a constant fashion," said Dr. Francesco Maura, a hematologist and researcher at Memorial Sloan Kettering Cancer Center in New York City who was not involved in the study. When chemo introduces mutations to blood cells, particularly blood stem cells, he said, "it doesn't necessarily mean the stem cell is aged; you just have more mutations." These chemo-induced mutations carry the same risk as age-related mutations, though — that is, their accumulation raises the risk of cancer.

Among the study participants, there was a 3-year-old who had chemo that carried 10 times the number of mutations in his blood than healthy, untreated kids his age. The toddler's blood cells looked older than those of an 80-year-old study participant who had never had chemo. But while mutation buildup makes cells look older, it doesn't always lead to tumor growth — just as not everyone who ages gets cancer.

The study had limitations, such as its small sample size. The researchers conceded that studying blood in test tubes could have skewed the results, because it doesn't fully recreate the human body's environment. Mitchell said her group would like to run similar experiments with a larger cohort and with circulating blood, but there are no plans to do so immediately.

Mitchell pointed to her and her colleagues' work published in 2024 in the journal The Lancet Oncology as an example of where this sort of research could go. They'd demonstrated that an alternative chemo combination for Hodgkin lymphoma worked just as well as the standard option while causing fewer knock-on mutations.

Hodgkin lymphoma has a high cure rate of more than 80%, but for other types of cancers with lower cure rates, applying this approach may be more challenging. Additionally, secondary tumors take years to develop, so people need to survive for some time following their initial treatment to encounter them. Optimizing their initial chemo drugs to minimize mutations wouldn't be helpful if the survival rates for their cancer aren't high.

In Maura's words, "first, you have to cure [that type of] cancer. Then you work toward reducing the toxicity of the treatment."

This article is for informational purposes only and is not meant to offer medical advice.

Blood plasma can harbor DNA changes that could flag cancer years before existing diagnostic tests, an early study hints.

The recent study, published May 22 in the journal Cancer Discovery, found traces of free-floating DNA from dead precancerous or cancerous cells in plasma that had been donated three years before a diagnosis.

"It's an important step toward preclinical cancer detection, which could potentially revolutionize cancer screening," said Catherine Alix-Panabières, a cancer researcher at the University of Montpellier in France who was not involved with the work. "Earlier detection typically correlates with better outcomes across many cancer types due to earlier intervention," she told Live Science in an email.

The prognosis for cancer patients generally grows worse the later their disease is caught, especially once it has grown and spread to other tissues. Yet the gene changes, or mutations, that give rise to tumors tend to appear decades beforehand. Consultant oncologist Dr. Yuxuan Wang at Johns Hopkins University and her colleagues wanted to see if they could detect tumor DNA in plasma long before cancer manifests.

They examined plasma — the liquid that blood cells are suspended within — that was collected from patients roughly 40 years ago for an unrelated study. They focused on 26 participants who had developed cancer within six months of donating blood, as well as 26 controls who did not develop cancer for at least 17 years post-donation.

Related: Simple blood tests could be the future of cancer diagnosis

Wang's group found between one and three common cancerous mutations in seven of the plasma samples, all of which were taken from participants that developed cancer within four months of donating blood.

Six of these patients had also donated blood between 3.1 and 3.5 years beforehand, so Wang's team turned back the clock further and assessed those earlier samples for the same mutations. Two of the early samples contained the same DNA errors, confirming that these warning signs were detectable years before the tumors appeared, at least in some people.

Since they found only a few common mutations in two of the six plasma samples taken three years before diagnosis, they then sequenced the plasma DNA to find additional mutations that were unique to each patient. Using the genomes of their white blood cells — a type of immune cell — as a reference, they found between four and 90 unique mutations in the plasma DNA from three patients. All told, they found hints of cancer in three of the five early samples they examined.

The patients in this study had a variety of cancers, including breast, colon, liver, lung, pancreas, and rectal cancer. However, it's not clear if the testing method works equally well for all tumor types. "Some organs will shed tumor DNA more than others," Wang told Live Science, noting that the blood-brain barrier, a protective membrane, may prevent brain cancer DNA crossing out of the organ and into the bloodstream.

In addition, the new research didn't find any cancer DNA in 18 of the 26 participants who developed tumors in the months after their samples were collected. That's not ideal for a clinical test, Wang said. But she suggested that detection could potentially improve if doctors took larger volumes of plasma from each patient.

Since the test could potentially detect cancer years before symptoms first appear, it could one day be useful for screening patients preemptively. However, further experiments are needed to ensure this diagnostic doesn't lead to false positive results, which could unnecessarily alarm patients and possibly lead to unnecessary treatments or invasive diagnostic procedures, like biopsies.

"Ethically, implementing such tests in routine screening would require clear guidelines on how to handle incidental findings," Alix-Panabières said.

And because the study only included plasma samples from 52 people, larger investigations involving hundreds or thousands of participants would be needed to validate the test before doctors could use it with confidence. "Realistically, widespread clinical adoption may take another 5–10 years," Alix-Panabières predicted.

Finding personalized mutations requires sequencing the patient's DNA, which can cost several hundred or thousands of dollars, Wang said. So even if such a test can be validated in larger trials, it's "probably not going to be something we can provide for everyone who we want to screen," and the test may need to be reserved for at-risk groups whose families have known histories of cancer, for instance.

The recent study consisted mostly of Black and white men and women between the ages 45 to 64 from four U.S. states. Future investigations could explore the efficiency of the test in people from other, genetically diverse backgrounds.

This article is for informational purposes only and is not meant to offer medical advice.

A toxic fungus, once thought to have caused fatal lung infections in tomb explorers, may hold the key to powerful new cancer treatments, new research suggests.

Within months of the discovery of the tomb of King Tutankhamun in 1922, the earl who had financed the excavation and visited the "wonderful" burial site died, leading many to believe the mummy had cursed those who entered the tomb. In the 1970s, 10 of the 12 archaeologists excavating the 15th-century crypt of King Casimir IV in Poland also met a similar fate.

Analysis of Casimir's tomb revealed the presence of a fungus called Aspergillus flavus, the toxins of which are known to cause a deadly lung infection.

Now, the same fungus has shown promise as a treatment for leukaemia, according to a new study published in Nature Chemical Biology. The researcher team identified and engineered a class of molecules within the fungus, called asperigimycins, that kill leukemia cells in a laboratory setting.

"This is nature's irony at its finest," study senior author Sherry Gao, a professor of chemical and biomolecular engineering at the University of Pennsylvania, said in a statement. "The same fungus once feared for bringing death may now help save lives."

Aspergillus flavus produces spores that are able to lie dormant for centuries — including inside sealed tombs. When disturbed, the fungus can cause deadly respiratory infections, particularly in people with weakened immune systems.

Related: College student discovers psychedelic fungus that eluded LSD inventor

In their new study, the scientists examined the unique chemical compounds produced by the fungus and discovered a class of natural compounds called RiPPs (ribosomally synthesized and post-translationally modified peptides). These molecules are difficult to isolate and rarely seen in fungi, but they hold therapeutic promise due to their complex structures and bioactivity. This means they have intricate, unique shapes that can interact with biological systems in powerful ways, such as killing cancer cells.

"We found four novel asperigimycins with an unusual interlocking ring structure," lead author Qiuyue Nie, a researcher in chemical and biomolecular engineering at the University of Pennsylvania, said in the statement. "Two of them had strong anti-leukemia properties even without modification."

To enhance the drugs' effectiveness, the researchers attached lipid molecules similar to those found in royal jelly, the nutrient-rich substance that sustains queen bees. This enabled the drugs to enter cancer cells more efficiently, because lipids help drugs cross cellular membranes, which are made largely of fats themselves.

Further analysis revealed how a gene called SLC46A3 acts as a kind of molecular gateway, helping the drug escape cellular compartments and target leukemia cells directly. This discovery could aid in the delivery of other promising but hard-to-administer drugs in the future.

Unlike broad-spectrum chemotherapy agents that can damage healthy cells, asperigimycins appear to specifically disrupt leukemia cell division without affecting healthy tissues. Early tests also suggest the compounds have minimal effects on breast, liver, and lung cancer cells. According to the researchers, this selectivity is important for minimizing unwanted side effects.

In addition to asperigimycins, the team believe similar life-saving compounds may be hidden in other fungal species.

The team are planning to test asperigimycins in animal models, with the eventual goal of launching human clinical trials. And by scanning fungal genomes and exploring more strains of Aspergillus, they hope to unlock new treatments.

"The ancient world is still offering us tools for modern medicine," said Gao. "The tombs were feared for their curses, but they may become a wellspring of cures."

Some early-onset cancers — those that occur in people under age 50 — are on the rise in the United States.

This overall increase is due to a rise in 14 different types of cancers in younger people, according to a new analysis. The largest increases have occurred in breast, colorectal, kidney and uterine cancer diagnoses.

While the overall incidence of early-onset cancer is still low, these small increases could add up over time.

A rise of a few percent per year is "not a huge change in the number of diagnoses, because cancer is still rare at these ages," Miranda Fidler-Benaoudia, a cancer epidemiologist at Alberta Health Services and the University of Calgary, told Live Science. "But it's when it's happening over two, three decades that it really leads to a meaningful increase in that period."

The reasons behind these increases are complex and manifold, and many are probably specific to each type of cancer, experts say.

To tease out trends in early-onset cancer diagnoses and the myriad reasons behind them, National Cancer Institute epidemiologist Meredith Shiels and colleagues compiled data on cancers diagnosed in 15- to 49-year-olds between 2010 and 2019 in the U.S. In a study published May 8 in the journal Cancer Discovery, the team broke down changes in the rates of different cancers in three age groups: 15 to 29, 30 to 39, and 40 to 49.

Breast and uterine cancer rates increased in every early-onset age group, while rates of colorectal and certain kidney cancers increased among 30- to 39-year-olds and 40- to 49-year-olds, the team found. More than 80% of the additional cancers that occurred in 2019 compared with 2010 were one of these four types. Other diagnoses that increased in at least one early-onset cohort included melanoma, cervical cancer and stomach cancer, though incidences of these cancers remained low overall.

Lifestyle changes

Many factors could contribute to these observed increases. Research suggests that obesity is a risk factor for colorectal, kidney and uterine cancers, all of which are rising in younger people. Globally, the percentage of adults who are overweight or obese has increased significantly since 1990. Although most studies linking cancer and obesity were conducted in older adults, it's possible that higher rates of obesity in younger people could also increase the rates of early-onset cancer, the researchers wrote. One 2024 study suggests that more than half of uterine cancers diagnosed in 2019 might be linked to obesity.

Changes in reproductive patterns over the years could also be contributing to the increased incidence of early-onset breast cancers, Fidler-Benaoudia said. Girls are getting their periods earlier, and women are having fewer children, and having them later in life, than they did a few generations ago. Being younger at first menstruation, giving birth fewer times, and giving birth for the first time later in life have all been linked to a higher risk of developing certain types of early-onset breast cancer, the researchers wrote. Other research suggests that using oral contraceptives (birth control pills) might also slightly elevate the risk of early-onset breast cancer, though it may also protect against ovarian and endometrial cancers.

Better detection

Earlier detection of cancers in people with genetic risk factors may also play a role. For instance, those with certain BRCA gene variants have a higher risk of breast, ovarian or prostate cancer, while those with Lynch syndrome face an increased risk of myriad cancers, including colon cancer, stomach cancer and brain cancer.

Newer screening guidelines recommend people with these genes start screening for cancer earlier than those with an average risk of the disease. Even a small increase in the number of early-onset cancers detected via these new recommendations could trigger an uptick in diagnoses.

Screening for other, unrelated issues could also help identify certain cancers earlier. For example, changes in imaging procedures for MRIs and CT scans mean that health care professionals are catching more instances of renal cell carcinoma, a type of kidney cancer, during other tests. This incidental detection has led to an increase in kidney cancer diagnoses in almost all age groups, the researchers wrote.

Environmental exposures

People's prenatal or early-life exposures to certain compounds may also fuel specific early-onset cancers. Researchers reported in April in the journal Nature that childhood exposure to a chemical called colibactin, which is produced by certain E. coli strains in the colon, causes DNA mutations observed more frequently in early-onset colorectal cancers.

Showing that an exposure directly causes a certain type of early-onset cancer — or even pinpointing which types of exposures might pose a risk — is no easy feat. "I think that we need large studies that follow individuals over the life course, including at younger ages, to be able to identify risk factors for early-onset cancers," Shiels told Live Science in an email.

Even with these sorts of extended studies, though, it can be challenging to pin down the exact causes of early-onset cancer. "The issue with cancer at young ages is, whilst it's increasing, it's still relatively rare [compared] to those older age groups," Fidler-Benaoudia said. "To have enough people develop cancer to then identify risk factors in this prospective way is incredibly challenging, because you need huge, huge numbers."

While it's impossible to eliminate your individual risk of getting cancer, there are some things that reduce the overall risk at the population level. For instance, wearing sun protection and getting vaccinated against human papillomavirus (HPV) can help protect against certain cancers, Fidler-Benaoudia said. Similarly, limiting alcohol and smoking can reduce the odds of a person developing cancer at any point in their life, not just before age 50, Tomotaka Ugai, a cancer epidemiologist at the Harvard T.H. Chan School of Public Health and Brigham and Women's Hospital, told Live Science.

Researchers have found that a cocktail of two cancer drugs can increase the lifespan of mice by up to around 30%, according to a new study.

The two drugs, trametinib and rapamycin, were both effective at extending the lives of mice when administered separately, but offered even greater benefits when taken together. They also reduced chronic inflammation and delayed cancer development in the aging mice.

Mice are not humans, however, so the new findings don't necessarily mean that people will live longer by taking these drugs (outside of their current prescribed use). But the study authors noted that the drugs, which are approved by the U.S. Food and Drug Administration (FDA), are good candidates for human trials exploring ways to help older people age better.

The researchers published their study about the potential longevity benefits of the FDA-approved drugs on May 28 in the journal Nature Aging.

"While we do not expect a similar extension to human lifespans as we found in mice, we hope that the drugs we're investigating could help people to stay healthy and disease-free for longer late in life," study co-lead author Linda Partridge, a geneticist at University College London in the U.K. and the Max Planck Institute for Biology of Ageing in Cologne, Germany, said in a statement.

Both drugs work by targeting cell communication pathways in the body, which play a critical role in aging and the development of diseases like cancer. Rapamycin inhibits a protein called mTOR, which regulates the division and death of cells and is associated with cancer and other diseases. Trametinib disrupts a molecular pathway called RAS/Mek/Erk, which also plays a role in cancerous cell proliferation — again, useful if you're trying to stop the growth and spread of cancer cells.

Related: Heat waves may accelerate the aging process

Rapamycin was already known to extend the lifespan of mice, while trametinib has previously been shown to add time to the lifespan of flies. Previous studies have also found that the drugs' separate lifespan-extending effects stack in flies, providing an even greater boost when administered together. However, the new study marks the first time that scientists have combined rapamycin and trametinib to study aging in mammals.

The researchers mixed the drugs into the food of lab mice and found that, individually, rapamycin extended the mouse lifespan by 15% to 20% while trametinib extended it by around 5% to 10%. Just like in flies, the drugs proved stronger together, with a cocktail of the two increasing the mouse lifespan by up to 29%, according to the study.

To explore the biochemical underpinnings of these effects, the team took tissue samples from the mice and analyzed how the activity of their genes was affected by the two drugs. They found that not only did the mice gain separate benefits from the two different drugs but that, when used in combination, the drug cocktail influenced gene activity differently to when either drug was taken alone, according to the statement.

The study highlights that these two drugs could be good candidates for geroprotectors, which are an emerging class of drugs aimed at delaying the onset of diseases and improving the health of older people. However, for now, the researchers plan to optimize the use of trametinib to maximize its benefits while minimizing side effects like weight loss and liver lesions.

"Trametinib, especially in combination with rapamycin, is a good candidate to be tested in clinical trials as a geroprotector," co-lead author Sebastian Grönke, a senior postdoctoral researcher at the Max Planck Institute for Biology of Ageing, said in the statement. "We hope that our results will be taken up by others and tested in humans. Our focus is on optimising the use of trametinib in animal models."

Former President Joe Biden has been diagnosed with an "aggressive" form of prostate cancer, which has spread to his bones, his office announced Sunday (May 18).

The statement noted that Biden, 82, initially experienced urinary symptoms, and on examination, doctors had found a nodule in his prostate. On Friday (May 16), he was diagnosed with prostate cancer. The cancer was "characterized by a Gleason score of 9 (Grade Group 5) with metastasis to the bone," the statement said, as reported by BBC News. Once prostate cancer has spread to the bones, the survival rate drops significantly.

The severity of prostate cancer is ranked using Gleason scores between 6 and 10, with a higher number meaning that the cancer is more likely to grow quickly and spread to additional body parts, or "metastasize." These scores help doctors determine how best to treat a given patient's cancer. "While this [Biden's score] represents a more aggressive form of the disease, the cancer appears to be hormone-sensitive which allows for effective management," Sunday's statement said.

Here's what to know about prostate cancer, including what determines its severity and how it's treated.

Related: The 10 deadliest cancers, and why there's no cure

Androgen-depleting treatments can have some side effects. "These can potentially include an increase in the size of the breast, hot flushes, an increase in body fat and impotence," Porter said. Additionally, these hormone treatments can become less effective over time, as the cancer cells find ways to grow without sex hormones.

"Most cancers eventually become resistant to such treatments, entering a 'castration-resistant' phase where alternative approaches are needed," Stebbing said. "Early hormone-sensitive stages often respond well to targeted therapies, delaying progression."

Prostate cancer is also commonly treated using radiation therapy and surgical removal of the prostate, but prostate removal isn't typically used in people whose cancer has already spread to the bones. Again, prostate cancer that has spread to the bones cannot typically be cured, but the ACS notes that there are treatments that can inhibit further spread and improve quality of life.

This article is for informational purposes only and is not meant to offer medical advice.

A new artificial intelligence (AI) model can predict a person's biological age — the state of their body and how they're aging — from a selfie.

The model, dubbed FaceAge, estimates how old a person looks compared to their chronological age, or the amount of time that's passed since their birth. FaceAge's makers say their tool could help doctors decide on the best course of treatment for diseases like cancer. But one outside expert told Live Science that before it is used that way, follow-up data needs to show it actually improves treatment outcomes or quality of life.

When a doctor is treating a cancer patient, "one of the first things they do is they try to assess how well the individual is doing," Hugo Aerts, director of the AI in Medicine Program at Mass General Brigham, said in a news briefing on May 7. "This is often a very subjective assessment, but it can influence a lot of future decisions" about their treatment, including how aggressive or intense their treatment plan should be, he added. For example, doctors may decide a patient who looks younger and more fit for their age may tolerate an aggressive treatment better and eventually live longer than a patient who looks older and more frail, even if the two have the same chronological age.

FaceAge could make that decision easier by turning doctors' subjective estimates into a quantitative measure, the study authors wrote in the new study published May 8 in the journal Lancet Digital Health. By quantifying biological age, the model could offer another data point in helping doctors decide which treatment to recommend.

Aerts and his colleagues trained the model on more than 58,000 photos of people ages 60 years and older who were assumed to be of average health for their age at the time the photo was taken. In this training set, the researchers had the model estimate chronological ages and assumed that the people's biological ages were similar, though the scientists noted that this assumption is not true in every case.

The team then used FaceAge to predict the ages of more than 6,000 people with cancer. Cancer patients looked about five years older, on average, than their chronological ages, the team found. FaceAge's estimates also correlated with survival after treatment: The older a person looked, regardless of their chronological age, the lower their chances of living longer. By contrast, chronological age was not a good predictor of survival in cancer patients, the team found.

FaceAge isn't ready for hospitals or physicians' offices yet. For one, the dataset used to train the model was pulled from IMDb and Wikipedia — which may not represent the general population, and may also not account for factors like plastic surgery, lifestyle differences, or images that have been digitally retouched. Further studies with larger and more representative training sets are needed to understand how those factors impact FaceAge estimations, the authors said.

And the researchers are still improving the algorithm with additional training data and testing its efficacy for other conditions besides cancer. They're also investigating what factors the model draws on to make its predictions. But once it's finalized, FaceAge could, for example, help doctors tailor the intensity of cancer treatments like radiation and chemotherapy to specific patients, study co-author Dr. Ray Mak, a radiation oncologist at Mass General Brigham, said during the briefing. A clinical trial for cancer patients, comparing FaceAge to more traditional measures of a patient’s frailty, is starting soon, Mak added.

Ethical guidelines surrounding how FaceAge information can be used, such as whether health insurance or life insurance providers could access FaceAge estimates to make coverage decisions, should be established before rolling out the model, the researchers said. "It is for sure something that needs attention, to assure that these technologies are used only for the benefit of the patient," Aerts said in the briefing.

Doctors would also need to carefully consider when and how they use FaceAge in clinical settings, said Nicola White, a palliative care researcher at University College London who was not involved in the study. "When you're dealing with people, it's very different to dealing with statistics," White told Live Science. A long-term study assessing whether involving FaceAge in treatment decisions improved patients' quality of life is needed, she said.

The researchers noted the AI tool wouldn't be making calls about treatment on its own. "It's not a replacement for clinician judgement," Mak said. But FaceAge could become part of a physician's toolkit for personalizing a treatment plan, "like having another vital sign data point."

A parasite that infects millions across Africa may quietly prime the cervix for cancer — and, surprisingly, a standard treatment for the infection could amplify that risk, new research hints.

Schistosoma haematobium, a flatworm that lives in freshwater and can penetrate the skin, is already known to raise bladder cancer risk. Now, research presented April 12 at ESCMID Global 2025 — an annual meeting about clinical microbiology and infectious diseases — has uncovered how the worm can also trigger cancer-related gene activity in the cervix, both during an active infection and after it's been cleared.

The study included only a small group of women, so its results bear confirmation in larger trials.

"Further study is needed for us to understand if this link actually exists and to what extent it increases the risk of cervical cancer," said Dr. Joshua Cohen, the medical director of the gynecologic cancer program at City of Hope Orange County who wasn't involved in the research.

Regardless, "given parasitic infections are most common in countries with less access to clean water and sanitation, it is important to focus on reducing the rate of parasitic infections for all people living in these locations," Cohen told Live Science in an email.

Related: New self-swab HPV test is an alternative to Pap smears. Here's how it works.

An unsung factor in cervical cancer?

S. haematobium infects approximately 110 million people globally. However, previous studies conducted in African countries suggest only 1.7% to 3% of cervical cancer cases in those regions can be linked to the infection. The primary pathogen that drives cervical cancer is human papillomavirus (HPV); nearly all cervical cancer cases are linked to persistant infections with high-risk strains of the virus.

HPV drives cancer by producing viral proteins that disrupt cervical cells' life cycle and by worming its way into the infected host's DNA. S. haematobium, however, takes a different approach, Dr. Jennifer Downs, an associate professor of medicine at Weill Cornell Medicine who worked on the new research, told Live Science in an email.

The flatworm, found in Africa and some parts of the Middle East, causes a disease called schistosomiasis, which can lead to itchy skin, fever, chills, cough and muscle ache. To investigate how the worm might affect the cervix, researchers analyzed tissue samples from 39 women in Tanzania — 20 with active infections and 19 without.

All of the infected participants received the standard treatment, a drug called praziquantel. Tissue samples were collected before this treatment and then again four to 12 months later.

The team analyzed the tissues' gene activity, pinpointing several genes that behaved differently in infected women than in uninfected women; they also identified genes that changed their activity after the antiparasitic treatment. Four of the altered genes are known to play roles in cancer, typically by driving abnormal cell growth and tumors when their activity is turned up too high.

After treatment, genes involved in inflammation and tissue repair, along with genes associated with the breakdown of the cervix's protective barriers, became more active. These changes were tied to more blood-vessel growth and less cell death, as well as to the activation of some processes seen in cancer.

Changes in the genes that help maintain the cervix's protective barrier are "especially concerning," lead study author Dr. Anna Mertelsmann, a researcher at University Hospital Zurich and Weill Cornell Medicine who specializes in infectious diseases and molecular oncology, said in a statement. "Without these, women may become more vulnerable to HPV infection and persistence."

So, these changes in the cervix could open the door to cancer-causing viral infections.

How the worm raises cervical cancer risk

In summary, when the parasite's eggs become lodged in cervical tissue, they provoke a strong inflammatory response, Mertelsmann told Live Science in an email. This inflammation produces reactive molecules that could damage DNA in cells in the surface of the cervix, she explained.

The same mechanism is believed to lead to bladder cancer, which can occur when S. haematobium eggs enter the bladder, Downs said. An estimated 40% to 70% of women and girls infected with the parasite likely have eggs lodged in the genital tract, she added.

In addition to the carcinogenic effects of the eggs, the infection triggers repeated cycles of injury and healing that can lead to abnormal tissue growth, Mertelsmann said in an email. Simultaneously, changes in the cervix's protective barrier may impair the body's ability to detect and eliminate precancerous cells before they progress to cancer, she said.

The study also found that praziquantel may carry risks for cancer, as it was associated with genetic changes linked to the disease. "At least shortly after treatment, the elimination of the S. haematobium might at least transiently increase the risk for oncogenesis," or cancer growth, Mertelsmann told Live Science.

However, while the data point to these cancer-related genetic changes, "we don't know if S. haematobium infection or the treatment causes or contributes to cervical cancer," she emphasized. Longer, larger studies are needed to unpack exactly how the genetic changes might impact cancer risk, she said.

Notably, if left untreated, S. haematobium infection can damage organs, including the lungs, intestines and spleen, so forgoing treatment would come with its own risks.

The insights from this study could have significant implications for cancer prevention in regions where schistosomiasis is endemic.

"Women diagnosed with S. haematobium should be closely monitored for early signs of cervical tissue abnormalities," Mertelsmann said in the statement. Additional therapies, such as anti-inflammatory or immune-modulating drugs, may also help to counteract the harmful effects seen after treatment, she suggested. "Moreover, widespread HPV vaccination could play a crucial role in reducing cervical cancer risk for women affected by schistosomiasis," she added.

Now, the researchers are following a larger group of 180 women over a year to confirm these early results. Future studies will explore whether women with a history of schistosomiasis are more likely to develop cervical cancer due to long-term HPV infections.

This article is for informational purposes only and is not meant to offer medical advice.

There are tens of trillions of cells in the human body, and new cells are constantly forming as older cells age and die. But sometimes, cell growth and replication doesn't stop when it should. These abnormal cells multiply too quickly, harming healthy tissue and interfering with bodily functions. This runaway cell growth and accumulation of abnormal cells is called cancer.

There are more than 200 types of cancer, with about 20 million new cases of cancer diagnosed globally each year. The most common type of cancer worldwide is lung cancer, which causes 1.8 million deaths annually. Of any cancer, lung cancer kills the most people worldwide each year.

The earliest mention of cancer in Homo sapien history (though it was not yet called by that name) dates to about 3000 B.C. A medical textbook from ancient Egypt, known as the Edwin Smith Papyrus, documented eight cases of breast tumors. The term "cancer" arose during the first century A.D. from the Latin word for "crab," which refers to the shape of certain cancerous tumors.

Modern cancer treatment options vary depending on several factors, including the age and overall health of the patient; the type of cancer; and the stage of disease. For some cancers, doctors may recommend a single treatment strategy, while others can require multiple treatments.

Treatments include surgeries to remove cancerous growths; medications that target specific cancer proteins; and chemical or radiation therapies to shrink tumors and stop the cancer from spreading. For some cancers, there are also treatments that harness the patient's immune system to fight cancer, called immunotherapies.

Everything you need to know about cancer

Cancer glossary

• Tumor: A solid mass created by the uncontrolled growth of cells in a bodily tissue
• Biopsy: A procedure that removes small samples of body tissues or fluids for analysis
• Metastasize: When cancer cells spread from their place of origin to other parts of the body
• Complete remission: A person's cancer is responding to treatment, that they have no signs or symptoms of the disease, and there are no cancerous cells in their body that can be detected by a scan or a blood test
• Partial remission: A person's cancer treatment is working but that tests show some cancerous cells remain in the body

Cancer pictures

Discover more

—When is cancer considered cured, versus in remission?

—The 10 deadliest cancers, and why there's no cure

—What happens to cancer cells when they die?

A simple blood test could reveal who is at high risk of skin cancer recurrence after tumor-removal surgery.

The test can detect fragments of tumor DNA with a simple blood draw to reveal the lingering presence of Stage III melanoma — a metastatic form of the deadliest form of skin cancer — that can't be seen with CT scans. Although the test isn't perfect, it could help flag patients who need aggressive treatment because their cancer is likely to come back.

"We're envisioning the test being used to monitor patients over time (perhaps every month or couple of months in the first 1-3 years after surgery) for an early indication that the melanoma is recurring," study senior author Dr. David Polsky, a dermatologic oncologist at the New York University Grossman School of Medicine, told Live Science in an email.

If the test showed signs of tumor DNA, Polsky continued, the doctor might choose to use more advanced imaging techniques to search for small, easy-to-miss tumors, or they might move to a more aggressive treatment regimen that uses a combination of cancer drugs instead of just one, for example.

Related: Simple blood tests could be the future of cancer diagnosis

Melanoma is a cancer of melanocytes, a type of pigmented skin cell. It accounts for only 1% of skin cancers, but it causes the most skin cancer deaths because it can quickly spread to other organs, or metastasize. Early detection is one of the best ways to boost the likelihood of survival.

Polsky and his colleagues focused on Stage III melanoma, which is melanoma that has spread to nearby lymph nodes, where immune cells are made and stored. Doctors perform surgery to remove as much of the cancer as possible before starting medications to kill any remaining tumor cells.

Patients then get CT scans to look for any signs of recurrence, but some patients have tiny deposits of melanoma that are too small to be detected by CT. To catch those deposits earlier, Polsky and his team turned to circulating tumor DNA, or ctDNA. These are DNA fragments released from tumor cells during their normal life cycle. The fragments circulate in the plasma — the liquid portion of the blood — and can be detected by telltale mutations that are unique to cancer.

As part of a larger clinical trial of a combination of cancer drugs, the research team studied blood samples from 597 patients who had recently undergone surgery. The participants also had follow-up blood samples taken three months, six months, nine months and 12 months after either starting a treatment or receiving a placebo.

Immediately after surgery, 13% of the patients had detectable ctDNA in their blood plasma. Every single one of these patients experienced a cancer recurrence, the researchers found. Patients were also more likely to see their melanoma return when their ctDNA rose during the follow-up tests or if the ctDNA remained persistently high over the course of the testing.

The presence of the ctDNA predicted the return of the cancer 100% of the time; no one with a positive test escaped melanoma relapse. But the absence of ctDNA did not mean the patients were out of the woods. A negative test was correct 71% of the time in predicting that the person's cancer would not return. But some patients with no detectable ctDNA still saw recurrence.

"[T]he tests are highly accurate when they are positive, but not as accurate when they are negative," Polsky said.

The study's results were published April 15 in the journal The Lancet Oncology. The next step, Polsky said, is to make the test available to a clinical molecular pathology laboratory, where it can be used to make decisions about treatment. A clinical trial can then show whether using the blood test leads to better outcomes than not using them — a measure called "clinical utility."

"Demonstrating clinical utility of the test would be a major advance for the management of melanoma patients whose disease has spread beyond the skin," Polsky said.

Flashes of infrared light can detect signs of cancer in a patient's blood, new research suggests.

In a new study, scientists demonstrated that a test using infrared light can detect the difference between blood samples from patients with lung cancer and samples from those without the disease with up to 81% accuracy. They presented their findings in a study published April 9 in the journal ACS Central Science.

The new test is powered by artificial intelligence (AI) and examines differences in molecules found in blood plasma, the watery portion of blood that carries various proteins and chemical compounds — such as hormones and vitamins — around the body.

When blood samples are exposed to flashes of infrared light from a laser, the molecules held within the plasma vibrate. In turn, different components of the molecules absorb or reflect the energy from the light pulses, and consequently, they emit their own distinctive pattern of light that can be recorded and read as an "infrared molecular fingerprint."

Related: Detecting cancer in minutes possible with just a drop of dried blood and new test, study hints

The fingerprint differs between patients with cancer and those without the disease, the researchers reported. This suggests that the blood-screening method could offer a new approach to detecting cancer.

New blood tests are currently being developed to help diagnose a plethora of cancers, including those of the pancreas, breast and stomach. While still in the early stages of development, such tests aim to detect cancer earlier than current methods available, and they can achieve this in a less invasive way than traditional tissue biopsies, for instance.

"Laser-based infrared molecular fingerprinting detects cancer, demonstrating its potential for clinical diagnostics," study co-author Michaela Žigman, a scientist at the Max Planck Institute of Quantum Optics in Germany, said in a statement. With further development and testing in larger clinical studies, this approach could help advance cancer screening and diagnosis, she added.

To create the new blood test, Žigman and colleagues first trained an AI model to detect differences in the fingerprint of plasma samples from more than 2,100 people. This cohort included patients with lung, prostate, breast or bladder cancer who had not yet been treated for their disease. For each patient with cancer, the researchers showed the AI a blood sample from a person of the same sex and of a similar age who didn't have cancer, for comparison.

After training their AI model using these data, the researchers tested how accurate it was at identifying cancer fingerprints in the plasma of about 430 people who weren't included in the initial data. The researchers found that the model was up to 81% accurate at discerning plasma samples from patients with lung cancer compared with those from individuals without the disease.

However, the model was much less successful at detecting the other three types of cancer included in the study. For example, the model only detected around 50% of breast cancer cases.

Considering these limitations of the test, much more research will be needed before it could ever be used in clinical practice.

Nevertheless, the researchers behind the test are hopeful about its prospects. They now plan to train the model on a wider range of cancers, using data from more patients, to see if they can improve its accuracy in detecting cancer. They especially want to hone its ability to detect cancer at different stages of the disease, they said in the statement.