Prostate Cancer Research Today is a free monthly online journal that collates and summarizes the latest research about Prostate Cancer, including details on symptoms, genetics, screening, treatment, information. | ||||||||
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DNA copy number alterations in prostate cancers: a combined analysis of published CGH studies.Sun J, Liu W, Adams TS, Sun J, Li X, Turner AR, Chang B, Kim JW, Zheng SL, Isaacs WB, Xu J Center for Human Genomics, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157, USA. BACKGROUND: Identifying genomic regions that are commonly deleted or gained in neoplastic cells is an important approach to identify tumor suppressor genes and oncogenes. Studies in the last two decades have identified a number of common DNA copy number alterations in prostate cancer. However, because of various sample sizes, diverse tumor types and sources, as well as a variety of detection methods with various sensitivities and resolutions, it is difficult to summarize and fully interpret the overall results. METHODS: We performed a combined analysis of all published comparative genomic hybridization (CGH) studies of prostate cancer and estimated the frequency of alterations across the genome for all tumors, as well as in advanced and localized tumors separately. A total of 41 studies examining 872 cancers were included in this study. RESULTS: The frequency of deletions and gains were estimated in all tumors, as well as in advanced and localized tumors. Eight deleted and five gained regions were found in more than 10% of the prostate tumors. An additional six regions were commonly deleted and seven were commonly gained in advanced tumors. While 8p was the most common location of deletion, occurring in about a third of all tumors and about half of advanced tumors, 8q was the most commonly gained region, affecting about a quarter of all tumors and about half of all advanced tumors. CONCLUSIONS: The large number of tumors examined in this combined analysis provides better estimates of the frequency of specific alterations in the prostate cancer cell genome, and offers important clues for prioritizing efforts to identify tumor suppressor genes and oncogenes in these altered regions. Published 3 April 2007 in Prostate, 67(7): 692-700.
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