Rubin, Chinnaiyan, and colleagues at the University of Michigan have published extensive studies of molecular profiles of prostate cancer (Dhanasekaran et al., 2001). Using methods similar to those of Alizadeh et al., they classified carefully dissected prostate tissue specimens into normal adjacent tissue, benign prostatic hypertrophy, localized prostate cancer, and metastatic prostate cancer. Two control or comparison groups were utilized: first ,a commercial pool of normal prostates from men with no cancers, and second, normal adjacent prostate from men with prostate cancers. Each type of specimen was differentiated by the microarray clustering method, combined with arrays of prostate tissue from many patients. Many of the genes with substantial up- or downregulation fell into well-recognized categories of functions, including transcription factors, cell adhesion, p rotease/an ti-protease, phosphatase/kinase, free radical scavenger, and inflammation/ immunity genes (and protein products). Furthermore, prostate cancers that are responsive to anti-testosterone (estrogenic) therapy were differentiated from cancers that are nonresponsive or refractory to such therapy. They also identified a specific biomarker (Hepsin) that seems to have prognostic value for prostate cancers.
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