A gene, known as an androgen receptor (AR), is found in both prostate and breast cancers and has opposite effects on the two diseases, according to a recent study.
In breast cancer, the AR gene promotes cancer growth when the gene is “turned off.” However, in prostate cancer, the AR gene promotes cancer growth when the gene is “turned on.” Consequently, treating prostate and breast cancers require completely opposite approaches to AR. When it comes to prostate cancer, the treatment strategy should be to block AR. On the other hand, treatments for breast cancer should support AR production.
Researchers from Cleveland Clinic’s Lerner Research Institute, including Charis Eng, MD, PhD, Chair, Genomic Medicine Institute; Robert Silverman, PhD, and Warren Heston, PhD, both of the Department of Cancer Biology; studied whether the AR molecule indicated PTEN, the tumor suppressor protein.
The study revealed that AR inhibits PTEN expression in prostate cancer cells, yet stimulates it in breast cancer cells. The findings are published in the October 21, 2011, issue of Oncogene. Researchers determined that increased AR expression is associated with prostate cancer progression. Therefore, a common prostate cancer treatment strategy involves blocking AR, whereas AR supplementation is a strategy for treating breast cancer due to the fact that most breast cancers occur post-menopause, after AR production has ceased.
“We now see how androgen affects PTEN expression – and ultimately cancer,” said Dr Eng. “Our observations help explain why this prostate cancer risk can be halved by drinking red wine, which increases PTEN expression. Our data also suggest that treatment of the exact same cancer must be personalized for males and for females.”
Source: Cleveland Clinic.