Aberrant CpG island hypermethylation of multiple genes in colorectal neoplasia
Aberrant CpG island hypermethylation of multiple genes in colorectal neoplasia
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DOI：
10.1038/labinvest.3700108
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发表时间：
2004-07-01
影响因子：
5
通讯作者：
Kang, GH
中科院分区：
文献类型：
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作者：
Lee, S;Hwang, KS;Kang, GH
CpG岛高甲基化是一种潜在的灭活肿瘤抑制基因的手段，许多基因已被证明在结直肠癌中高甲基化和沉默。然而，关于结直肠癌及其前体病变中多个基因同时甲基化的数据有限。为了研究结直肠癌发生过程中多个基因甲基化谱的变化，我们使用甲基化特异性PCR方法研究了正常结肠（n=24）、结肠腺瘤（n=95）和结直肠癌（n=149）中12个基因（APC、COX-2、DAP-kinase、E-cadherin、GSTP1、hMLH1、MGMT、p14、p16、RASSF1A、THBS1和TIMP3）的甲基化。在正常结肠粘膜、腺瘤和癌中，这些基因甲基化的平均数量分别为0.12、1.8和3.0，呈逐步增加的趋势(P
CpG island hypermethylation is a potential means of inactivating tumor suppressor genes, and many genes have been, demonstrated to be hypermethylated and silenced in colorectal cancer. However, limited data is available upon the concurrent methylation of multiple genes in colorectal cancer and in its precursor lesion. To address changes in the methylation profiles of multiple genes during colorectal carcinogenesis, we investigated the methylation of 12 genes (APC, COX-2, DAP-kinase, E-cadherin, GSTP1, hMLH1, MGMT, p14, p16, RASSF1A, THBS1, and TIMP3) in normal colon (n=24), colon adenoma (n=95), and colorectal cancer (n=149), using methylation-specific PCR. The average number of these genes methylated per sample was 0.12, 1.8, and 3.0 in normal colon mucosa, adenoma, and carcinoma, respectively, showing a stepwise increase (P