Researchers at Weill Cornell Medical College, New York, have found the hormone estrogen plays a major role in about half of all prostate cancers. Their findings were published in the May 27 online edition of the Journal of the National Cancer Institute.

They have found that the estrogen-linked signaling helps drive a discrete and aggressive form of prostate cancer caused by a chromosomal translocation. This mutation causes the fusion of two genes.

The senior author, Dr. Mark A. Rubin, professor of pathology and laboratory medicine and vice chair for experimental pathology at Weill Cornell Medical College said “Fifty percent of prostate cancers harbor a common recurrent gene fusion, and we believe that this confers a more aggressive nature to these tumors. Interfering with this gene fusion — or its downstream molecular pathways — will be crucial in the search for drugs that fight the disease. Based on our new data, we now believe that inhibiting estrogen may be one way of doing so.”

Dr. Rubin first discovered and described the common fusions between the TMPRSS2 and ETS family member genes subset of prostate cancer in the journal Science in 2005. “The discovery showed that these malignancies occur after an androgen (male hormone)-dependent gene fuses with an oncogene — a type of gene that causes cancer,” he explains.

It is common knowledge that male hormones help spur prostate cancer, thus a first line treatment for prostate cancer recurrences is often androgen-deprivation therapy (ADT). Despite the ADT, prostate cancer usually will continue to progress. This simple reality clearly indicated that there are other molecular pathways a