Sharret Institute of Oncology, Hadassah-Hebrew University Medical Center, Kyriat Hadassah, POB 12000, 91120, Jerusalem, Israel.
Fam Cancer. 2010 Jun;9(2):141-50. doi: 10.1007/s10689-009-9298-9.
Mutations in DNA mismatch repair genes underlie lynch syndrome (HNPCC). Lynch syndrome resulting from mutations in MSH6 is considered to be attenuated in comparison to that caused by mutations in MLH1 and MSH2, thus more likely to be under diagnosed. In this study we report of a common mutation in the MSH6 gene in Ashkenazi Jews. Genetic counseling and diagnostic work-up for HNPCC was conducted in families who attended the high risk clinic for inherited cancer. We identified the mutation c.3984_3987dup in the MSH6 gene in 19 members of four unrelated Ashkenazi families. This mutation results in truncation of the transcript and in loss of expression of the MSH6 protein in tumors. Tumor spectrum among carriers included colon, endometrial, gastric, ovarian, urinary, and breast cancer. All but one family qualified for the Bethesda guidelines and none fulfilled the Amsterdam Criteria. Members of one family also co-inherited the c.6174delT mutation in the BRCA2 gene. The c.3984_3987dup in the MSH6 gene is a mutation leading to HNPCC among Ashkenazi Jews. This is most probably a founder mutation. In contrast to the c.1906G>C founder mutation in the MSH2 gene, tumors tend to occur later in life, and none of the families qualified for the Amsterdam criteria. c.3984_3987dup is responsible for 1/6 of the mutations identified among Ashkenazi HNPCC families in our cohort. Both mutations: c.3984_3987dup and c.1906G>C account for 61% of HNPCC Ashkenazi families in this cohort. These findings are of great importance for counseling, diagnosis, management and surveillance for Ashkenazi families with Lynch syndrome.
错配修复基因的突变是林奇综合征(HNPCC)的基础。与 MLH1 和 MSH2 突变导致的林奇综合征相比,由 MSH6 基因突变导致的林奇综合征被认为是衰减的,因此更有可能被误诊。在这项研究中,我们报告了一个在阿什肯纳兹犹太人中常见的 MSH6 基因突变。对遗传性癌症高危诊所就诊的家族进行了 HNPCC 的遗传咨询和诊断。我们在四个无关的阿什肯纳兹家族的 19 名成员中发现了 MSH6 基因中的 c.3984_3987dup 突变。该突变导致转录本截断,并导致肿瘤中 MSH6 蛋白表达缺失。携带者的肿瘤谱包括结肠癌、子宫内膜癌、胃癌、卵巢癌、膀胱癌和乳腺癌。除了一个家族之外,所有家族都符合贝塞斯达指南,但没有一个家族符合阿姆斯特丹标准。一个家族的成员还共同遗传了 BRCA2 基因中的 c.6174delT 突变。MSH6 基因中的 c.3984_3987dup 是导致阿什肯纳兹犹太人中 HNPCC 的突变。这很可能是一个创始人突变。与 MSH2 基因中的 c.1906G>C 创始人突变不同,肿瘤往往发生在生命后期,而且没有一个家族符合阿姆斯特丹标准。c.3984_3987dup 负责我们队列中阿什肯纳兹 HNPCC 家族中鉴定出的突变的 1/6。这两个突变:c.3984_3987dup 和 c.1906G>C 占本队列中阿什肯纳兹 HNPCC 家族的 61%。这些发现对阿什肯纳兹家族林奇综合征的咨询、诊断、管理和监测具有重要意义。