The University Record, September 4, 2001

Prostate cancer’s fingerprint revealed

By Sally Pobojewski
Medical School Communications

Normal prostate tissue, at top, has an organized structure. Cancerous tissue, at bottom, is completely disorganized. (Photo by Mark Rubin, Medical School)
Like most killers, prostate cancer leaves fingerprints. Every malignant cell has a unique pattern of active genes and proteins that spells the difference between benign, localized or metastatic tumors. Hidden in this molecular profile are answers to questions doctors hear every day: Is surgery really necessary? Can I afford to wait? Will the cancer come back?

Until now, physicians have been unable to decode these fingerprints, which hold the key to understanding the relationship between gene expression and future prognosis for men with prostate cancer. But a new study from the Medical School, published in the Aug. 23 issue of Nature, offers scientists their first look at the genetic and molecular profile of prostate cancer.

“Our study has important applications in the diagnosis, prognosis and treatment of prostate cancer,” says Mark Rubin, associate professor of pathology and urology, a co-author of the Nature paper. “The ultimate goal is to help physicians determine which involved in the development and progression of prostate cancer—each controlling a different step in the process.”

While some of the genes identified in the study are well known to cancer researchers, many others have never before been associated with prostate cancer. Two of these new genes are hepsin and pim-1, which could turn out to be important new clinical biomarkers for prostate cancer, according to Rubin.

“Without the U-M’s prostate tissue bank this work would not have been possible,” says Rubin. “We were also fortunate that U-M is one of only three medical schools in the United States with a rapid autopsy program where tissue samples are obtained within hours of death,” adds Chinnaiyan.

According to Chinnaiyan, the next step is determining the functional role for each gene identified in the study as having an association with prostate cancer. “This paper will generate a great deal of work for researchers in many laboratories,” he predicts.

“It has been 15 years since the Prostate Specific Antigen (PSA) test became available in 1987,” says Rubin. “This approach could give us many new diagnostic tests within three to five years. Eventually, it could lead to a diagnostic kit physicians could use to determine the best treatment and prognosis for their patients with prostate cancer.”