PITTSBURGH, July 15 According to a study published in the July 15 issue of the Journal of Clinical Oncology, genes expressed in benign tissue adjacent to prostate cancer tissue are much more similar to those expressed in prostate cancer tissue than previously thought. This finding, the first of its kind, may help predict populations both at risk for prostate cancer and for disease progression based on gene expression patterns, say researchers at the University of Pittsburgh.

"It is not clear what molecular events are responsible for the progression of prostate cancer to a lethal form of the disease," said Jian-Hua Luo, M.D., Ph.D., senior author of the study and assistant professor, department of pathology, University of Pittsburgh School of Medicine. "But by exploring the biology of prostate cancer through the identification of genes and patterns of gene expression, we can more precisely understand what genetic changes cause the disease to progress and develop therapeutic targets to prevent its progression at an earlier stage."

In the study, Dr. Luo, also director of the gene array laboratory at the University of Pittsburgh, and colleagues used high throughput quantitative analysis to genetically profile prostate cancer tissue and noncancerous prostate tissue samples. They analyzed 152 human tissue samples including 66 samples of prostate cancer tissue, 60 samples of benign prostate tissue adjacent to the tumor, 23 samples of donor prostate tissue free of genitourinary disease and three prostate cancer cell lines. Through the analysis, the researchers identified a set of 671 genes whose expression levels were significantly altered in prostate cancer tissue compared to disease-free tissue and found that patterns of gene expression in benign adjacent prostate tissue were much more similar to prostate cancer tissue than to disease-free tissue.

According to Dr. Luo, the gene expression patterns of benign adjacent tissue were
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Contact: Clare Collins
CollCX@upmc.edu
412-647-3555
University of Pittsburgh Medical Center
15-Jul-2004

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