作者: Stephen B. Baylin , James G. Herman , Sanna K. Myöhänen
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摘要: Inactivation of p16ink4A and other tumor suppressor genes has been associated with promoter region hypermethylation in neoplasia. However, direct proof for aberrant DNA methylation as an independent event loss gene function difficult to obtain. We addressed this question the colon carcinoma cell line HCT116, which contains one allele a coding frameshift mutation wild-type allele. Neither proximal region. The allele, but not mutant is hypermethylated, only expressed. Transcription from methylated/wild-type was restored after treatment demethylating agent 5-aza-2'-deoxycytidine. Thus, neoplastic cells, stable allele-specific transcription may arise nonmutated region, identifying mechanism inactivation.