Cancer history and loss of MSH2 and MLH1 protein expression in patients with endometrial hyperplasia

被引:3
作者
Maruyama, A
Saito, T
Hachitanda, Y
Tsukamoto, N
机构
[1] Kyushu Natl Canc Ctr, Gynecol Serv, Minami Ku, Fukuoka 8111395, Japan
[2] Kyushu Natl Canc Ctr, Pathol Serv, Minami Ku, Fukuoka 8111395, Japan
关键词
endometrial hyperplasia; hereditary nonpolypoid colorectal cancer; MSH2; MLH1; personal and family histories of cancer;
D O I
10.1046/j.1525-1438.2003.13190.x
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
In order to evaluate the hereditary background of endometrial hyperplasia patients in relation to protein expression of DNA mismatch repair genes, we evaluated 69 patients with endometrial hyperplasia and 18 patients with normal endometrium having both a personal and family history of cancer (two hereditary nonpolypoid colorectal cancer (HNPCC) patients). We obtained personal and family histories of cancer for all patients. MSH2 and MLH1 protein expression was investigated by immunohistochemical methods. In the endometrial hyperplasia patients, 11 had personal histories and 40 had family histories of cancer. Among the 11 endometrial hyperplasia patients with a personal history of cancer, most cancers were breast or colorectal cancers (82%). In the 40 patients with a family history of cancer, colorectal cancer (33%) was the most frequent. The incidence of loss of expression of MSH2 and/or MLH1 protein in endometrial hyperplasia patients with personal (64%) or family (40%) histories was significantly higher than that in patients without such history (no personal: 21% and no family: 10%; P = 0.0035 and 0.0065). No protein loss was detected in any of the cases with normal endometrium having either a personal or family history of cancer. Our results suggest that a portion of endometrial hyperplasia cases having a personal or family history of cancer may belong to HNPCC, and that in these cases, abnormality of the mismatch repair system may be an early event in endometrial carcinogenesis.
引用
收藏
页码:352 / 360
页数:9
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