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Telomeres and Prostate Cancer in African American Men

For years in Discovery, we’ve reported on the troubling facts — many of them determined from research done here at Johns Hopkins — that African American men are more likely to get prostate cancer, to have more or higher-grade cancer than was originally suspected, to have cancer recurrence after treatment, and more likely to die of their cancer compared to white men. (One of these stories features Ted Schaeffer’s latest findings here.)


Even when diagnosed with very low-risk prostate cancer, African American men are more likely to develop a tumor in a differ ent location, often in the anterior of the prostate, and these tumors ar e often high-grade and large in volume. But why? What makes African American men, out of all men in the w orld, the group hardest hit by prostate cancer? Christopher Heaphy, Ph.D., Assistant Professor of Pathology, the Dr. and Mrs. Peter S. Bing Scholar, offers new insight. “Our laboratory studies long stretches of specialized DNA located at the ends of every chromosome,” he says. “These protective caps of the chromosomes are called telomeres, and they stabilize the ends of the chromosomes.” Telomeres are a lot like aglets — the little bits of plastic at the tips of shoelaces — in that they protect chromosomes from getting frayed and tangled. “Unfortunately,” Heaphy says, “a portion of telomeric DNA gets lost from each chromosome end every time a cell divides . If too much of it is lost, then the telomere loses its protective function, and the cell’s chromosomes become unstable.” Heaphy and colleagues, Elizabeth Platz, Angelo De Marzo, and Alan Meeker, recently conducted a large study of the removed prostate tissue in men who underwent radical prostatectomy.


“Using a robust assay, we measured telomere lengths specifically in prostate cancer cells, and also in normal cancer-associated prostate stromal cells,” he explains. “Interestingly, we found that men with telomere abnormalities in both their prostate cancer cells and in the normal stromal cells nearby had a 14-fold higher risk of dying from their disease.” Heaphy notes that these findings w ere independent of the usual markers — Gleason score, stage of cancer, and PSA levels — that help determine pr ognosis. Now, in a follow-up collaboration with Ted Schaeffer, Heaphy and colleagues are proposing “that critical telomere shortening is an important causal factor in prostate tumor formation.”


They suspect that “African American men either inherit short telomeres, or they display an increased propensity for telomere shortening within the prostate.” Heaphy believes these telomere abnormalities may be a “distinct underlying biological factor” that can help explain the racial differences, including where tumors are likely to develop, and the greater severity of prostate cancer in African American men. The next step is to study what he calls the “mechanistic underpinnings” of this link between telomere abnormalities and prostate cancer racial disparities, “with the goal of opening new avenues for the development of preventive and therapeutic interventions.”

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