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Mutation and expression analysis of the p73 gene in prostate cancer
Author(s) -
Yokomizo Akira,
Mai Ming,
Bostwick David G.,
Tindall Donald J.,
Qian Junqi,
Cheng Liang,
Jenkins Robert B.,
Smith David I.,
Liu Wanguo
Publication year - 1999
Publication title -
the prostate
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.295
H-Index - 123
eISSN - 1097-0045
pISSN - 0270-4137
DOI - 10.1002/(sici)1097-0045(19990501)39:2<94::aid-pros3>3.0.co;2-w
Subject(s) - prostate cancer , prostate , exon , tumor suppressor gene , biology , gene , cancer research , allele , pca3 , mutation , gene expression , cancer , chromoplexy , microbiology and biotechnology , genetics , carcinogenesis
BACKGROUND p53 is the most highly mutated tumor suppressor gene in human cancers. Recently, p73, a first homologue of p53, was identified and considered to be an imprinted tumor suppressor gene. Thus, we analyzed the possible role of p73 in human prostate cancers. METHODS We investigated the expression levels and expressed allelotypes and searched for mutations in the p73 gene in 27 primary prostate cancers with matched normal tissues as well as in four prostate cell lines. RESULTS Allelic expression analysis using polymorphisms in exons 2 and 5 revealed that p73 is biallelically expressed in both normal and tumor tissues, suggesting that p73 is not imprinted in prostate tissues. Quantitative PCR demonstrated that p73 expression is the same in both normal and tumor prostate tissues. Denaturing high‐performance liquid chromatography and DNA sequencing revealed that there were no tumor‐specific mutations in the p73 gene at the genomic level. CONCLUSIONS These data indicate that alterations of p73, including mutations, changes in message abundance, and changes in allelic expression, are likely to be rare in early‐stage prostate cancer, and that p73 could be a tissue‐specific imprinting gene. Prostate 39:94–100, 1999. © 1999 Wiley‐Liss, Inc.