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Gastric Carcinogenesis and Underlying Molecular Mechanisms: Helicobacter pylori and Novel Targeted Therapy.

The oxygen-derived free radicals that are released from activated neutrophils are one of the cytotoxic factors of Helicobacter pylori-induced gastric mucosal injury. Increased cytidine deaminase activity in H. pylori-infected gastric tissues promotes the accumulation of various mutations and might p...

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Published in:BioMed Research International Vol. 2015; pp. 1 - 8
Main Authors: Nishizawa, Toshihiro, Suzuki, Hidekazu
Format: review tables/charts Journal Article
Published: Wiley-Blackwell 4/7/2015
Online Access:View this record in EBSCOhost
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      jtl: BioMed Research International
      issn: 23146133
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    pubinfo:
      dt: 4/7/2015
      vid: 2015
      pid: 480
      pub: Wiley-Blackwell
      place: Malden, Massachusetts
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        109273907
        109273907
        109273907
        10.1155/2015/794378
        109273907
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        atl: Gastric Carcinogenesis and Underlying Molecular Mechanisms: Helicobacter pylori and Novel Targeted Therapy.
      aug:
        au:
          Nishizawa, Toshihiro
          Suzuki, Hidekazu
        affil: Division of Gastroenterology and Hepatology, Department of Internal Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan
      sug:
        subj:
          Helicobacter Infections Complications
          Helicobacter Pylori
          Gastric Mucosa Microbiology
          Stomach Neoplasms Physiopathology
          Stomach Neoplasms Therapy
          Mutation
          Genes
          Cytotoxins
          Epithelial Cells
          Gene Expression
          RNA
          Stomach Neoplasms Etiology
          Oxidative Stress
          Gastric Mucosa Pathology
          Epidermal Growth Factors
          DNA Methylation
          Stem Cells
          Models, Biological
      ab: The oxygen-derived free radicals that are released from activated neutrophils are one of the cytotoxic factors of Helicobacter pylori-induced gastric mucosal injury. Increased cytidine deaminase activity in H. pylori-infected gastric tissues promotes the accumulation of various mutations and might promote gastric carcinogenesis. Cytotoxin-associated gene A (CagA) is delivered into gastric epithelial cells via bacterial type IV secretion system, and it causes inflammation and activation of oncogenic pathways. H. pylori infection induces epigenetic transformations, such as aberrant promoter methylation in tumor-suppressor genes. Aberrant expression of microRNAs is also reportedly linked to gastric tumorogenesis. Moreover, recent advances in molecular targeting therapies provided a new interesting weapon to treat advanced gastric cancer through anti-human epidermal growth factor receptor 2 (HER-2) therapies. This updated review article highlights possible mechanisms of gastric carcinogenesis including H. pylori-associated factors.
      pubtype: Academic Journal
      doctype:
        review
        tables/charts
        Journal Article
      ougenre: Article
    language: English
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