Promoter methylation of tumor-related genes in gastric carcinogenesis

摘要: Aberrant promoter methylation and subsequent silencing of cancer-related genes has been recognized as an important pathway involved in gastric carcinogenesis. In fact, several factors are believed to contribute its induction epithelia, including aging, diet, chronic inflammation infection Helicobacter pylori (H. pylori) Epstein-Barr virus (EBV). However, the underling mechanisms not completely identified, despite belief that increased expression or activity DNA methyltransferases (DNMTs), decreased demethylation may excessive methylation. A great number with have observed cancer (GC), among which p16INK4A (p16), Mut L homologue 1 (MLH1), Epithelial-cadherin (E-cadherin), Runt-related transcription factor 3 (RUNX3), adenomatous polyposis coli (APC), O(6)-methylguanine-DNA methyltransferase (MGMT), Ras association domain family 1A (RASSF1A) Death-associated protein kinase (DAPK) extensively studied. Unlike distinct characterization single genes, analysis multiple provide more information risk prediction, early detection, prognosis assessment chemotherapy choice for GC. Specifically, particular monitoring screening should be performed on those over 45 years old, precancerous disease H. EBV. As alternative tumor tissues, detection patient sera washes also used prediction detection. what still poses a challenge well puzzle is determination very analysis. Because epigenetic alterations normally reversible, drugs chemical compounds demethylating activity, such 5-aza-2'-deoxycytidine (5-aza-dC) could treatment patients gene view adverse effects 5-aza-dC, DNMT-targeted strategy proposed prove effective than agents.