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Molecular mechanisms of gastric cancer initiation and progression by Helicobacter pylori

Servetas, Stephanie L.; Bridge, Dacie R.; Merrell, D. Scott

Current Opinion in Infectious Diseases: June 2016 - Volume 29 - Issue 3 - p 304–310
doi: 10.1097/QCO.0000000000000248
PATHOGENESIS AND IMMUNE RESPONSE: Edited by Dennis L. Stevens
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Purpose of review 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.

Recent findings 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.

Summary 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.

Department of Microbiology and Immunology, F. Edward Hébert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland, USA

Correspondence to D. Scott Merrell, PhD, Department of Microbiology and Immunology, F. Edward Hébert School of Medicine, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, MD 20814, USA. Tel: +1 301 295 1584; e-mail: douglas.merrell@usuhs.edu

* Stephanie L. Servetas and Dacie R. Bridge contributed equally to the writing of this article.

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