It's quick and easy to access Live Science Plus, simply enter your email below. We'll send you a confirmation and sign you up for our daily newsletter, keeping you up to date with the latest science news.
Dr. David Samadi is chairman of urology and chief of robotic surgery at Lenox Hill Hospital in New York City, and a board-certified urologist and oncologist specializing in the diagnosis and treatment of prostate cancer, urologic diseases, kidney cancer and bladder cancer. He developed the Samadi Modified Advanced Robotic Technique (SMART) surgery to perform nearly 6,000 robotic prostate surgeries, and is one of the few urologic surgeons in the United States trained in oncology, open, laparoscopic and robotic surgery. Samadi contributed this article to Live Science's Expert Voices: Op-Ed & Insights.
Two decades ago, the notion of a woman preemptively having her breasts or ovaries surgically removed to fend off a genetic threat of cancer would have been preposterous. And yet, Angelina Jolie-Pitt and others in her predicament are now rightly supported in their attempt to dodge the disease, efforts once considered drastic.
A landmark new study may prompt prostate removal surgery to become similarly embraced for men facing crushing odds of dying of this disease. The new research uncovered actionable genetic mutations in 9 of 10 advanced-prostate-cancer patients, including some of the same BRCA mutations which predispose some women to gynecological cancers.
The seminal research, published recently in the journal Cell, has been hailed as prostate cancer's "Rosetta Stone." It dramatically decodes the genetic language of the disease, advancing precision-medicine efforts. A global group of researchers, led in the United Kingdom by scientists at the Institute of Cancer Research, used tumor biopsy samples from 150 patients. These individuals had so-called metastatic castration-resistant prostate cancer — an incurable, lethal form — that had spread to distant sites in the body and stopped responding to standard, hormone-based treatments.
About 90 percent of the men with this aggressive prostate cancer harbored mutations in their tumors that could be targeted by new or existing cancer drugs, according to the study, the first to analyze in depth the genomic landscape of this intractable malignancy. Additionally, 14 percent of patients carried a mutation in the BRCA1 or BRCA2 gene, already notorious for contributing to a daunting hike in the risk of breast and ovarian cancers. Another 8 percent were found to have an inherited genetic predisposition to developing prostate cancer.
Study authors contend that the findings could help doctors find these "clinically actionable" mutations — and offer drug combinations targeting them — in advanced prostate cancer patients. This could be done with routine genomic testing in this group. Indeed, a class of drugs known as PARP inhibitors, already part of the drug arsenal used to combat BRCA-positive breast and ovarian cancers, seems a solid candidate to treat prostate cancers that have the same mutation. Researchers also said the study could make a case for offering genetic screening to men with a family history of prostate cancer.
Sign up for the Live Science daily newsletter now
Get the world’s most fascinating discoveries delivered straight to your inbox.
Individual genomic testing is key
These outcomes are perfectly logical and attainable. But I believe this important new information begs us to do even more.
In addition to performing genomic testing on tumors from patients who have incurable prostate cancer, the same should be done for all prostate malignancies. I've long maintained that lower-grade and higher-grade prostate tumors are essentially two different diseases, even though they both fall under the definition of prostate cancer. [5 Things You Should Know About Prostate Cancer ]
Genomic testing could definitively distinguish between the two, steering doctors to use less invasive and toxic treatments for some, while using the necessary full arsenal of therapies — including surgery, radiation, chemotherapy and hormone treatments — for others. Mapping the genetic blueprint for each man's prostate tumor would minimize the guesswork in effectively treating his disease, maximizing the ideals of precision medicine.
If you're a topical expert — researcher, business leader, author or innovator — and would like to contribute an op-ed piece, email us here.
Beyond that, men with a family history of prostate cancer, or those whose mothers, sisters or aunts have tested positive for BRCA mutations, can proactively seek genetic testing to unearth any genetic predispositions lurking in their own DNA. Some of the men from this admittedly small subgroup may choose to preemptively have their prostate glands removed to prevent a cancer diagnosis.
Preemptive removal would be a radical step, to be sure, and not one that any man would undertake lightly. But I've treated many with metastatic prostate cancer who I'm sure would have been grateful for this type of knowledge, which might have spared their lives.
The vast similarities between breast and prostate cancers are rarely appreciated. By the numbers, the diseases are nearly identical. Both strike about 230,000 Americans and kill about 30,000 each year. Both are the most common malignancies diagnosed in their respective genders, with surgery considered the definitive treatment in early disease. And this new research has underscored that breast and prostate cancers even share some of the same genetic mutations.
Now, physicians should expand our thinking to include another link between the two: considering preemptive removal of these nonessential body parts when genetic testing predicts overwhelming odds of developing or dying from cancers originating there. This groundbreaking new study underscores how our decision-making abilities are much enhanced by genetic mapping; we would be wise to heed the call.
Follow all of the Expert Voices issues and debates — and become part of the discussion — on Facebook, Twitter and Google+. The views expressed are those of the author and do not necessarily reflect the views of the publisher. This version of the article was originally published on Live Science.
Live Science Plus
