Rethinking Prostate Cancer Screening

A conversation with Dr. Hari, prostate cancer researcher at the Rutgers University Cancer Institute.

Dr. Hari Iyer is an assistant professor at the Rutgers Cancer Institute. A recent prostate cancer study that he co-authored revealed how access to care and environmental exposure shape survival rates in men with prostate cancer. The study followed 103,067 U.S. veterans who, through the Veterans Association (VA), had a prostate biopsy between 2015 and 2023, examining how their earlier prostate-specific antigen (PSA) screening related to what that biopsy found.

Men who were older at their first PSA test, and who let more time pass between tests, were significantly more likely to be diagnosed with metastatic prostate cancer rather than localized or benign disease. Veterans who began screening before age 50 with shorter intervals had roughly a tenth the metastatic rate of those who started at 60 or older with longer gaps. Few men had that most favorable screening pattern, which the authors say leaves room to optimize screening.

He spoke with Superpower about the major findings in his study, where he sees the future of prostate cancer screening going, and his recommendations for understanding one’s individual risk.

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Q:  Ten percent of new diagnoses are in men 55 and younger. Why aren't younger men getting tested?

A:  Prostate cancer is generally a disease of older men. In our data, four out of five cases are in men 50 and over, so with limited resources, the healthcare system tends to focus its messaging there. But the field is moving away from a one-size-fits-all “every man on the same schedule” toward tailored screening based on risk. Black and African American men are at higher risk and are often diagnosed younger, so there's now discussion about starting screening conversations in their 40s rather than the more common 55-and-older recommendation.

There's also a strong genetic contribution to prostate cancer risk — genes like BRCA1 and BRCA2, and mutations in the chromosome 8q24 region that are more prevalent in men of African ancestry. One of our VA colleagues, Dr. Jason Vassy, is leading one of the first genetics-informed screening trials, to see whether using that information to get the highest-risk men into care earlier, regardless of age, actually improves outcomes.

Q:  Your study found Black men were somewhat overrepresented among those diagnosed. What does that tell us?

A:  In our data, of the men who had a biopsy, the Black population was actually slightly more likely to be diagnosed with localized (more favorable, treatable) disease and less likely to fall in the benign group. So the interpretation isn't that Black men are less likely to be diagnosed; it's that among those diagnosed, more of them had favorable cancers. That's not what you typically see in population-based cohorts.

The VA is unique. Because of its social supports and the fact that it isn't a fee-for-service model, it helps underrepresented, minoritized populations get easier access. And when that access barrier goes away, some of the stark Black-white mortality disparities we see in nationwide studies are substantially attenuated.

Q:  You also studied environmental exposures. Where does something like Agent Orange fit in?

A:  Agent Orange was a chemical used in sprays during the Vietnam War to kill foliage, and it appears carcinogenic in animal and cell studies. It's of great interest to veterans, who encounter many chemical exposures in service. The challenge is that exposure was recorded not at a detailed individual level but by broad categories like where someone was stationed, and the military calls it a “presumptive exposure.” When a presumed exposure is tied to a benefit, there's an incentive to find the diagnosis, which creates a messy causal problem.

With my collaborator Dr. Isla Garraway, we ran one of the largest studies and found a strong association, but I'd stop short of calling it causal. Still, even as a signal of future risk, it could be useful for tailoring screening in that group.

Q:  Are there genetic tests that tell you your prostate cancer risk, like for breast and ovarian cancer?

A:  Some of the same mutations, like BRCA, are relevant, though the prostate cancer genes may differ somewhat. The complicated part is personal: genetic tests aren't perfect predictions. They tell you that, on average, people with a mutation have some higher risk. Some people really want to know; others would rather not, and deal with it if it comes. That's exactly the kind of thing to work through with your doctor.

Even for someone who'd rather not know, if the mutation, the family history, and other signs all point to a case where catching it early clearly helps, that's still worth knowing.

Q:  It's just a blood test, so why aren’t PSA screenings part of a routine annual checkup at 40 or 45?

A:  Because no screening test is perfect. Ideally a test would catch everyone who'll get the disease and clear everyone who won't, but statistically that's impossible. You either catch people who don't have it or miss people who do, and the PSA test has real problems here. Many men who test positive go on to biopsy and even treatment when, had the test never been done, they'd have died of something else. These are often older men, and getting them totally focused on prostate cancer can do more harm than good.

This actually happened: when PSA testing spread indiscriminately in the 1980s and '90s, there was a massive spike in diagnoses. That wasn't an epidemic, it was overtesting. In hindsight, many of those men likely never needed the diagnosis or the treatment that followed.

Q:  What PSA level signals concern, and why does testing over time matter?

A:  For most of the time I've studied this, four nanograms per milliliter has been the cut point where a provider would say we need to do more workup. But that's an average, and it means different things at different ages. The real value is testing over your life rather than once.

If your PSA is very low — say zero to one — in your 40s, there's a good chance it won't budge, and men who stay low generally aren't likely to progress to advanced cancer. I'd love to see that framed as reassurance, not just alarm: a low, stable value can be genuinely good news, and we've all got plenty else to worry about.

Q:  What recent advances are improving how prostate cancer is detected?

A:  Two big ones. First, PSMA-based scans (PSMA is a protein useful for monitoring prostate cancer) are being used more for imaging and guiding treatment. Second, and most promising, is adding imaging to reduce unnecessary biopsies. The PSA blood test is good at finding cancer, but it produces a lot of false positives (due to finding high levels from inflammation or some other enlargement). So, many men go through a biopsy who don't actually have a serious cancer.

Using MRI sometimes with AI algorithms that scan thousands of images to help decide whether a biopsy is even warranted should cut down on that harm. It may also make screening more palatable: It's a very different conversation to tell someone, “You just need to sit for a scan, nobody's going inside you,” than to send them for a biopsy. That could increase uptake among younger, higher-risk men.

Q:  What's the bottom line from your study? What should men take away?

A:  Our paper found that starting screening younger, having a lower PSA at the start, and shorter intervals between tests were all associated with lower risk of metastatic disease. That's not brand new, but we showed it holds in a contemporary population. These are also easy things to discuss with a physician: your age, your PSA value today and how it's changing, and how often you should be screened.

More broadly, this is the most commonly diagnosed cancer in men, one in five cancer diagnoses, so it's worth understanding. Reflect on your family history; if a father, grandfather, or uncle had it, that's a reason to talk to your doctor. And the usual advice still holds: Eating well, exercising, sleeping, and keeping a healthy weight are all associated with a lower risk of the more aggressive tumors.

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This interview has been edited and condensed for clarity.

Dr. Hari Iyer

Assistant Professor, Cancer Epidemiology and Health Outcomes, Rutgers Cancer Institute of New Jersey

Assistant Professor, Department of Medicine – Division of Medical Oncology, Robert Wood Johnson Medical School

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