Mitochondrial Dysfunction May Account for Poor Prostate Cancer Outcomes in Black Americans

Mitochondrial Dysfunction May Account for Poor Prostate Cancer Outcomes in Black Americans

Prostate cancer health disparities between blacks and whites in the U.S. are well-documented, with studies demonstrating higher incidences of the cancer and poorer response to treatments among African-American men. Now, a new report suggests that mitochondrial problems in blacks with prostate cancer may account for their resistance to chemotherapy.

The study, “Mitochondrial dysfunction-mediated apoptosis associates with defective heat shock protein response in African-American men with prostate cancer,” was published in the British Journal of Cancer.

“In an earlier study, we provided the first evidence that African-American men possess reduced levels of mitochondrial genetic material in healthy prostate tissues, compared to Caucasian-American men. This new study highlights the importance of mitochondrial dysfunction as one of the main reasons for prostate cancer health disparities,” Dhyan Chandra, PhD, an associate professor of Oncology in the Department of Pharmacology and Therapeutics at Roswell Park Cancer Institute (RPCI), said in a press release. “We conclude that the presence of severe mitochondrial dysfunction in African-American men with prostate cancer, compared with Caucasian men with the disease, would be one of the potential reasons for the increased cancer resistance to chemotherapy and the recurrence of disease.”

Mitochondria are a key cellular component in the apoptotic pathway, and mitochondria malfunction is often associated with resistance to chemotherapy, hampering tumor destruction or leading to cancer relapse. Consistently, the research team from Buffalo has shown that African-American men are at higher risk of disease spread because mitochondria dysfunction in prostate cancer cells make them more resistant to chemotherapy.

Restoration of mitochondrial activity in cancer cells using the small molecule dichloroacetate can induce tumor cell death and decrease tumor growth in many cancers. However, when the researchers treated prostate cancer cells isolated from African-American men with this molecule, few effects on cell proliferation were seen, compared to a strong suppression in the proliferation of Caucasian-American-derived cells, because dichloroacetate did not restore mitochondrial activity to the required levels.

Results highlight the need for new anticancer agents that better restore mitochondrial function in African-American patients, which would help control the disease.

“These findings may provide an explanation for the higher incidence and mortality rates of prostate cancer among African-American men. African-American patients might get more positive outcomes after major restoration of mitochondrial function, which could improve the anticancer effects of therapy,” Dr. Chandra said.

Added Willie Underwood III, MD, an associate Professor in the Department of Urology and a study co-author, “Although these findings are extremely insightful, more basic and clinical studies are needed to understand their impact in reaching our goal of eliminating the racial disparities in prostate cancer mortality.”

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