title: [cag PAI and gastric carcinogenesis-association with p53 gene mutation].
abstract: It is widely accepted that carcinogenesis is a multistep process in which regulation of both cell proliferation and apoptosis is disturbed. p53, which is considered the cellular gatekeeper for growth and division, induces apoptosis. Helicobacter pylori(Hp) infection is an accepted risk factor for the development of gastric cancer, but not all infected individuals develop gastric cancer. Because CagA+ Hp induces increased cell proliferation, the CagA+ strain is believed to play an important role in the pathogenesis of gastric cancer. We have reported that p53 alteration were more frequently found in the CagA+ Hp infection in gastric cancer patients. In this chapter, we summarized recent findings of the relation among p53, CagA and cag PAI.
authors.affiliation: Department of Gastroenterology, Tokai University School of Medicine.
authors.forename: Ryuzo
authors.initials: R
authors.lastname: Deguchi
authors.forename: Tetsuya
authors.initials: T
authors.lastname: Mine
authors.forename: Takeshi
authors.initials: T
authors.lastname: Miwa
authors.forename: Atsushi
authors.initials: A
authors.lastname: Takagi
mesh_terms: D000942:Antigens, Bacterial; D001426:Bacterial Proteins / Q000235:genetics*; D016480:Helicobacter pylori / Q000235:genetics*; D006801:Humans; D009154:Mutation; D013274:Stomach Neoplasms / Q000235:genetics*; D016159:Tumor Suppressor Protein p53 / Q000235:genetics*
chemical_list: D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D016159:Tumor Suppressor Protein p53; C080866:cagA protein, Helicobacter pylori