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pubmed-article:9788441pubmed:abstractTextDeletion of the q23-24 region of human chromosome 10 is one of the most frequent genetic alterations in prostate cancer, suggesting that inactivation of a tumor suppressor gene in this region is involved in the development or progression of this carcinoma. A candidate gene, PTEN/MMAC1, has been identified from this chromosomal region; mutations of this gene have been found in various advanced tumors and cell lines including those of prostate cancer. To further define the role of PTEN/MMAC1 in the development of prostate cancer and its spectrum of genetic alterations, we analysed 40 pT2 or pT3 prostate tumors for allelic loss, mutations, and homozygous deletions using PCR-based methods. Six tumors showed loss of heterozygosity for one of the ten markers analysed, while one tumor showed loss of two markers. None of the markers within PTEN/MMAC1 was lost. Direct sequencing of PCR amplified exons and intron/exon junctions of all 40 tumors revealed three sequence variants, one of which was a point mutation in exon 9, while the other two were polymorphisms. Using multiplex PCR, no homozygous deletions were detected in any of the neoplasms. Our results showing a low frequency of alterations of PTEN/MMAC1 in pT2 and pT3 prostate cancers suggest that this gene plays an insignificant role in the development of most low stage carcinomas of the prostate.lld:pubmed
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pubmed-article:9788441pubmed:articleTitlePTEN/MMAC1 is infrequently mutated in pT2 and pT3 carcinomas of the prostate.lld:pubmed
pubmed-article:9788441pubmed:affiliationDepartment of Pathology, University of Virginia Health Sciences Center, Charlottesville 22908, USA.lld:pubmed
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pubmed-article:9788441pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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