MSH2 DEFICIENT MICE ARE VIABLE AND SUSCEPTIBLE TO LYMPHOID TUMORS
MSH2 DEFICIENT MICE ARE VIABLE AND SUSCEPTIBLE TO LYMPHOID TUMORS
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DOI：
10.1038/ng0995-64
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发表时间：
1995-09-01
期刊：
影响因子：
30.8
通讯作者：
MAK, TW
中科院分区：
文献类型：
--
作者：
REITMAIR, AH;SCHMITS, R;MAK, TW
人类MSH 2基因（细菌MutS错配修复基因的同源物）的改变与大多数遗传性非息肉病性结肠癌（HNPCC）病例共分离。我们已经产生了纯合子MSH 2（+）小鼠。令人惊讶的是，这些小鼠被发现是可行的，产生的后代在孟德尔的比例，并通过至少两代繁殖。从两个月大开始，纯合-/-小鼠开始高频率地发展含有微卫星不稳定性的淋巴肿瘤。这些数据建立了MSH 2缺陷和癌症发病机制之间的直接联系，这些突变小鼠应该是研究肿瘤进展以及筛选致癌和抗癌药物的良好模型。
Alterations of the human MSH2 gene, a homologue of the bacterial MutS mismatch repair gene, co-segregate with the majority of hereditary non-polyposis colon cancer (HNPCC) cases. We have generated homozygous MSH2(+) mice. Surprisingly, these mice were found to be viable, produced offspring in a mendelian ratio and bred through at least two generations. Starting at two months of age homozygous -/- mice began, with high frequency, to develop lymphoid tumours that contained microsatellite instabilities. These data establish a direct link between MSH2 deficiency and the pathogenesis of cancer, These mutant mice should be good models to study the progression of tumours and also to screen carcinogenic and anti-cancer agents.