Molecular mechanisms of gastric cancer initiation and progression by Helicobacter pylori

Current Opinion in Infectious Diseases
Stephanie L ServetasD Scott Merrell

Abstract

Infection with the Gram-negative, microaerophilic pathogen Helicobacter pylori results in gastric cancer in a subset of infected individuals. As such, H. pylori is the only WHO classified bacterial class I carcinogen. Numerous studies have identified mechanisms by which H. pylori alters host cell signaling pathways to cause disease. The purpose of this review is to highlight recent studies that explore mechanisms associated with induction of gastric cancer. Over the last year and a half, new mechanisms contributing to the etiology of H. pylori-associated gastric cancer development have been discovered. In addition to utilizing the oncogenic CagA toxin to alter host cell signaling pathways, H. pylori also induces host DNA damage and alters DNA methylation to perturb downstream signaling. Furthermore, H. pylori activates numerous host cell pathways and proteins that result in epithelial-to-mesenchymal transition and induction of cell survival and proliferation. Mounting evidence suggests that H. pylori promotes gastric carcinogenesis using a multifactorial approach. Intriguingly, many of the targeted pathways and mechanisms show commonality with diverse forms of cancer.

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Citations

Oct 15, 2020·International Journal of Molecular Sciences·Shamshul Ansari, Yoshio Yamaoka
Mar 17, 2021·Biochemical Genetics·Diba Borzabadi FarahaniMohammad Reza Fattahi
Aug 14, 2021·Clinical & Translational Oncology : Official Publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico·A A KhanP Cash

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Methods Mentioned

BETA
biopsies
transfection
nuclear translocation

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