作者: Jill A. Macoska , Isaac J. Powell , Wael Sakr , Mary-Ann Lane
DOI: 10.1016/S0022-5347(17)37504-3
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摘要: Genetic alterations of multiple loci that serve as markers for the induction and progression disease have been identified in several adenocarcinomas, but not adenocarcinoma prostate. To determine if similar genetic occur prostate carcinoma could extent clinical disease, we examined 23 predominantly moderately-differentiated, localized carcinomas one prostatic dysplasia changes structure copy number ten selected genes. These genes include 1) those important to androgen metabolism prostate, receptor steroid 5 alpha reductase genes; 2) map 10q (PLAU) 7q (MET) chromosomal regions found deleted some carcinomas, 3) proto-oncogenes (ERBB2, INT2, MYC) tumor suppressor gene (RB1, TP53 D17S5) altered adenocarcinomas breast, colon lung. Gene were detected specimen, a lymph node metastasis from poorly differentiated tumor. This specimen exhibited loss heterozygosity two putatively active suppression, D17S5, on short arm chromosome 17. study indicates gross evident be used development well- or lesions, 17p region may useful marker advanced