作者: Raquel Seruca , Nuno R. Santos , Leonor David , Miguel Constáncia , Helena Barroca
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摘要: Mutations in recently identified genes on chromosomes 2 and 3 seem to be responsible for repair errors (RER+) throughout the genome. This novel genetic mechanism was first reported hereditary non-polyposis colorectal cancer syndrome cancers that are characteristic of this syndrome, such as carcinomas right colon, stomach endometrium. We investigated frequency RER+ phenotype a series 34 sporadic gastric carcinomas, an attempt see if cases displayed any particular morphologic features and/or they showed distinctive clinicopathologic characteristics. Twelve loci were investigated. found 23 RER- (67.6%) 11 (32.4%). A significant association between localization tumors: 9 (81.8%) located at antrum whereas all cardiac tumors RER-. The also significantly related presence moderate/abundant T-cell lymphoid infiltration within tumors. 3-year survival rate patients with suggestively longer than No relationship several characteristics cases, including age, sex, staging, histologic type ploidy, despite trend towards advanced age poorly differentiated, intestinal carcinomas. high microsatellite instability supports involvement carcinogenesis. Gastric tend occur differentiated adenocarcinomas elderly patients, display abundant carry relatively good prognosis. © 1995 Wiley-Liss, Inc.