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Press Releases

October 10, 2018

In Black Men, Baseline Screening in Midlife Strongly Predicts Aggressive Prostate Cancer

First study focusing on this population addresses important research gap

Black men are more likely to be diagnosed with, and to die from, prostate cancer yet recommendations about prostate cancer screening are primarily based on studies of white men. A new study led by investigators at Brigham and Women’s Hospital and Harvard T.H. Chan School of Public Health is the first to look at results exclusively among black men and to address whether an optimized screening strategy with baseline prostate specific antigen (PSA) levels predict prostate cancer in this population. The study finds that baseline PSA levels measured at midlife strongly predicted risk of total and aggressive prostate cancer in black men years in the future. Results are published online in European Urology.

“We found that a single, baseline PSA level measured during midlife strongly predicted subsequent diagnosis of total and aggressive prostate cancer up to 12 years after a blood draw,” said co-lead author Mark Preston, MD, MPH, a urologic surgeon in the Division of Urology at BWH. “Our findings suggest that targeted screening based on a midlife PSA might identify black men at high risk of aggressive prostate cancer while minimizing screening in those at low risk.”

“Black men in the U.S. are 2.5 times more likely to die of prostate cancer compared to white men, yet screening studies to date have largely been focused on white men,” said co-lead author Lorelei Mucci, MPH, ScD, associate professor of Epidemiology at the Harvard T.H. Chan School of Public Health. “As such, the data from our study address a critical gap in understanding the substantial racial disparities and suggests a potential strategy to reduce prostate cancer death in black men.”

The research team took a targeted, risk-stratified approach, leveraging data on men enrolled in the federally funded Southern Community Cohort Study (SCCS), a collection of 86,000 men and women from the Southeastern U.S., that included more than 22,000 black men. The team performed a nested, case-control study of 197 men, ages 40 to 64, who developed prostate cancer, including 91 cases of aggressive disease, and compared them to 569 matched controls.

The team found that 95 percent of total and 97 percent of aggressive prostate cancer cases had baseline PSA above the average for their age group. Compared to men with PSA at or below the age-specific median, men with levels above the median had significantly increased risk of aggressive prostate cancer across age groups. Men with PSA levels above the 90th percentile had the greatest risk.

The authors noted that increased risk was seen with PSA levels that were higher than the average but still well within the “normal” range – and low enough not to trigger follow-up in usual clinical practice.

“These findings do not imply that prostate biopsy or definitive treatment is immediately required in younger men with higher PSA levels at baseline, as this could lead to over-diagnosis, but that they undergo more intensive PSA screening to enable earlier identification of cancer and potential cure while still possible,” the authors write.

Co-authors of this study hold or are named on patents related to a statistical method to detect prostate cancer, receive royalties from sales of this test and own stock in companies to which these patents have been licensed. Additional details about financial disclosures can be found in the paper. This work was supported by the Dana-Farber/Harvard Cancer Center Mazzone Awards Program, the Dana-Farber/Harvard Cancer Center SPORE in Prostate Cancer (P50 CA090381), Prostate Cancer Foundation Young Investigator Awards, an American Urological Association Urology Care Foundation Scholar Award., and a post-doctoral grant from AFA Insurance supported in part by NIH T32 CA 009001. Additional funding support was provided from the National Cancer Institute [R33 CA127768, P50 CA92629, P30 CA008748, U01 CA199338-02]; the National Institute for Health Research (NIHR) Oxford Biomedical Research Centre Program in UK, the Swedish Research Council [VR-MH project nr. 2016-02974], the Swedish Cancer Society [CAN 2017/559]; the Sidney Kimmel Center for Prostate and Urologic Cancers; David H. Koch through the Prostate Cancer Foundation