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// Nianshuang Li 1,* , Chuan Xie 1,* and Nong-Hua Lu 1 1 Department of Gastroenterology, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China * These authors have contributed equally to the review and writing of this manuscript Correspondence to: Nong-Hua Lu, email: // Keywords : Helicobacter pylori; p53; tumourigenesis Received : May 08, 2016 Accepted : August 13, 2016 Published : August 19, 2016 Abstract Helicobacter pylori ( H. pylori ) is an ancient and persistent inhabitant of the human stomach that is closely linked to the development of gastric cancer (GC). . Emerging evidence suggests that H. pylori strain interactions with gastric epithelial cells subvert the best- characterized p53 tumour suppressor pathway. A high prevalence of p53 mutations is related to H. pylori infection. H. pylori also accelerates p53 protein degradation by disturbing the MDM2-P53 feedback loop. Additionally, H. pylori triggers the alteration of other p53 isoforms. Dysregulation of p53 by H. pylori infection contributes to gastric carcinogenesis by mediating cell proliferation and apoptosis. This review focuses on the regulation of p53 in H. pylori infection-associated GC.
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Li et al. (2016) studied this question.
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