title: [Genetic and epigenetic alterations in gastric carcinogenesis].
abstract: Genetic and epigenetic alterations are induced during gastric carcinogenesis. Infection by H. pylori markedly increases induction of both alterations, and inflammation triggered by the infection is critical for induction of aberrant DNA methylation (epigenetic alterations). Oncogenes, such as PIK3CA, CTNNB1, KRAS, and ERBB2, are activated by point mutations and gene amplification. Tumor-suppressor genes, such as TP53, CDH1, CDKN2A, and MLH1, are inactivated by mutations, and more frequently by aberrant methylation if they have promoter CpG islands. The information on the activated signaling pathway, such as the ERBB2-MAPK signaling pathway, is now becoming useful for patient stratification. Comprehensive analysis of genetic and epigenetic alterations in gastric cancers is expected to lead to more occasions of translation.
authors.affiliation: Division of Epigenomics, National Cancer Center Research Institute.
authors.forename: Toshikazu
authors.initials: T
authors.lastname: Ushijima
authors.forename: Satoshi
authors.initials: S
authors.lastname: Yoshida
mesh_terms: D019175:DNA Methylation / Q000235:genetics*; D044127:Epigenesis, Genetic; D016481:Helicobacter Infections / Q000235:genetics; D016480:Helicobacter pylori; D006801:Humans; D009857:Oncogenes / Q000235:genetics*; D017354:Point Mutation / Q000235:genetics; D013274:Stomach Neoplasms / Q000235:genetics