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Dr. Mark Preston discusses prostate cancer screening

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"The goal here is obviously to identify men who need investigation and diagnosis of prostate cancer and who we don't need to biopsy at all," says Mark A. Preston, MD, MPH.

In this video, Mark A. Preston, MD, MPH, discusses his approach to prostate cancer screening. He is senior author of the recent Journal of Urology study, “Free PSA and Clinically Significant and Fatal Prostate Cancer in the PLCO Screening Trial.” Preston is a urologic surgeon at Brigham and Women’s Hospital and an assistant professor of surgery at Harvard Medical School in Boston, Massachussets.

Transcription:

Based on these findings, are you likely to alter your approach to prostate cancer screening?

Personally, I incorporate a number of factors into screening practices—obviously, the total PSA, but we're also looking at what the age is. There are normal values for PSA based on your age; whether you're 45, 55, 65, for example, so that factors into what a screening practice would be. In addition would be the PSA change over time; essentially, the PSA density, if that's information that we know. I've used free PSA for years, which is part of the impetus for studying it in more detail. There's always a number of new biomarkers that are coming along that sometimes use a combination of free PSA with other things, but we wanted to study that by itself. I think it should be incorporated in screening practices in general. It's cheap and readily available. Pretty much all hospital labs do it; as opposed to just checking the box for PSA, check the boxes for PSA and free PSA. That gives you that additional data point.

To give you a bit of a background on free PSA, PSA is a protein that's produced by the prostate. It goes up for a number of different reasons: a big prostate, cancer, inflammation. What is unique about PSA is that some of it is free floating and some of it is bound to protein, and that ratio can help predict if that PSA elevation is more likely due to prostate cancer or benign prostate growth. For example, if the free-to-total ratio is greater than 25, it's more likely that PSA is due to benign prostate growth. If it's less than 10, then it's more likely that it's due to cancer. Now, no marker is perfect; you have to use that within the overall setting. But those breakdowns were actually very helpful in predicting whether high-grade cancer was present. What we found was that men with a free-to-total ratio that was less than 10% had significantly worse clinically significant prostate cancer rates, but also prostate cancer-free survival as well, compared with those men who had a ratio that was greater than 25%. For example, we looked at the cumulative incidence of fatal prostate cancer—those are the men who developed fatal prostate cancer over the 15 years that followed - and if their PSA was above 2, and their free-to-total ratio was less than 10%, that cumulative incidence of fatal prostate cancer was 3.2%. However, if their free-to-total ratio was greater than 25%, it was 0.03%. So there's a tremendous separation in risk in men with a PSA above 2, so you can use that to risk stratify in greater detail and decide who needs closer follow-up or investigation with biopsy or who can just be followed with PSAs more regularly. The goal here is obviously to identify men who need investigation and diagnosis of prostate cancer and who we don't need to biopsy at all. Decreasing rates of biopsy and the potential side effects of that is important nationwide.

This transcript was edited for clarity.

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