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Alteration of DNA methylation in gastrointestinal carcinogenesis
Author(s) -
Fang Jing Yuan,
Xiao Shu Dong
Publication year - 2001
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1046/j.1440-1746.2001.02554.x
Subject(s) - dna methylation , methylation , carcinogenesis , epigenetics , epigenetics of physical exercise , cpg site , cancer research , biology , cancer epigenetics , epigenomics , microbiology and biotechnology , dna , gene , genetics , gene expression
DNA methylation is the main epigenetic modification in humans. The methylation of promoter inhibits the transcription in most genes. In normal tissues, isolated CpG dinucleotides in bulk chromatin are often methylated, whereas cytosines in CpG islands are unmethylated. In neoplasms including gastrointestinal cancer, this pattern of methylation is commonly reversed. The alteration of DNA methylation plays a key role in the process of carcinogenesis. The gastrointestinal carcinogenesis is suggested to be associated with the decrease of total genomic DNA methylation; hypomethylation of certain specific oncogenes such as c‐myc, c‐Ha‐ras, c‐fos and α‐fetoprotein; and hypermethylation of the promoter of some tumor suppressor genes containing p16 INK4A , E‐cadherin and hMLH1 genes. This review focuses on the analysis methods for methylation, studies for aberrant DNA methylation in gastrointestinal carcinogenesis, and the intervention changing methylation, including the treatment of 5‐azacytidine, supplement of folate and gene therapy.