Prostate Cancer's Genetic Fingerprint

One in six American men are diagnosed with prostate cancer within their lifetime and 186,000 will be diagnosed this year. For most men, their disease is confined to the prostate gland, making it easier to treat and less lethal. However, some unfortunate patients suffer from a more aggressive cancer that metastasizes, or spreads beyond the boundaries of the prostate gland.

Physician-scientists are trying to uncover part of the disease's molecular fingerprint, with the hope of explaining why some forms metastasize. Their findings may help physicians provide tailored, and therefore, more effective treatments for patients.

Dr. Mark A. Rubin, professor of pathology and laboratory medicine, and vice chair for experimental pathology at Weill Cornell Medical College, and attending pathologist at NewYork-Presbyterian Hospital/Weill Cornell Medical Center, believes that the common joining of two genes to form a new fusion gene influences a certain type of prostate cancer that is more aggressive and sensitive to hormones. In a recent article published in the Journal of the National Cancer Institute, Dr. Rubin describes how in addition to the male hormone testosterone, estrogen — typically thought of as a female hormone — can stimulate this fusion gene. Dr. Rubin's group is currently exploring how this mechanism may help us understand how aggressive prostate cancer progresses in the absence of male hormones.

Currently, Dr. Rubin and his colleague Dr. Francesca Demichelis, assistant professor in pathology and laboratory medicine and computational biomedicine at the Institute of Computational Biomedicine at Weill Cornell Medical College, are testing blood samples and comparing the DNA of over 2,500 men with and without prostate cancer. They hope to discover clear genetic indicators of prostate cancer, especially its aggressive forms. Their findings will potentially lead to the development of diagnostic tests and preventive drugs for prostate cancer.