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1Oq23.3 loss of heterozygosity is higher inlymph node-positive (PT2-3,N+) versus lymph node-negative (PT2-3,N0) prostate cancer

Loss of heterozygosity (LOH) in the region of 1Og23.3 has beenassociated with multiple tumors, including glioblastoma multiforme, melanoma, endometrial carcinoma, and prostate carcinoma. The tumor suppressor gene, PTEN/MMAC1, is also located in this region, and, in addition to other tumor types (eg,...

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Bibliographic Details
Published in:Human pathology 2000-04, Vol.31 (4), p.504-508
Main Authors: Rubin, Mark A., Gerstein, Amy, Reid, Kris, Bostwick, David G., Cheng, Liang, Parsons, Ramon, Papadopoulos, Nickolas
Format: Article
Language:English
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Summary:Loss of heterozygosity (LOH) in the region of 1Og23.3 has beenassociated with multiple tumors, including glioblastoma multiforme, melanoma, endometrial carcinoma, and prostate carcinoma. The tumor suppressor gene, PTEN/MMAC1, is also located in this region, and, in addition to other tumor types (eg, glioblastoma multiforme, endometrial, and melanoma), PTEN/MMAC1 mutations have been found in prostate cancer cell lines, xenografts, and hormone refractory prostate cancer tissue specimens. The aim of this study was to evaluate LOH at 1Oq23.3 as a marker of cancer progression in node-positive prostate cancer. Genetic alterations in the region of 1Oq23.3 were assessed in 23 node-positive (pT2-3, N+) and 44 node-negative prostate (pT2-3, NO) cancers with D10S532, D10S1687, D10S541, and D10S583 flanking polymorphic genetic markers; PTENCA, a genetic marker within PTEN/MMAC1, was also tested. Using DNA from paired normal and microdissected tumor samples, LOH at microsatellite loci was determined after polymerase chain reaction amplification. LOH in at least 1 marker was identified in 14% (6 of 44) of lymph node-negative and 43% (10 of 23) of lymph node-positive prostate cancers (chi-square test, P = .007). This increase in genetic alterations in node-positive prostate cancer suggests that 1Oq23.3 is a marker for metastatic progression.
ISSN:0046-8177
1532-8392
DOI:10.1053/hp.2000.6713