作者: Peter W Laird , Laurie Jackson-Grusby , Amin Fazeli , Stephanie L Dickinson , W Edward Jung
DOI: 10.1016/0092-8674(95)90329-1
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摘要: We have used a combination of genetics and pharmacology to assess the effects reduced DNA methyltransferase activity on ApcMin-induced intestinal neoplasia in mice. A reduction Min mice due heterozygosity gene, conjunction with weekly dose inhibitor 5-aza-deoxycytidine, average number adenomas from 113 control only 2 polyps treated heterozygotes. Hence, contributes substantially tumor development this mouse model neoplasia. Our results argue against an oncogenic effect hypomethylation. Moreover, they are consistent role for generation C T transitions seen at high frequency human colorectal tumors.