Molecular mechanisms of gastric cancer initiation and progression by Helicobacter pylori. Issue 3 (June 2016)

• Record Type: Journal Article
• Authors: Servetas, Stephanie L.; Bridge, Dacie R.; Merrell, D. Scott
• Is Part Of: Current opinion in infectious diseases. Volume 29:Issue 3(2016)
• Page Start: 304
• Page End: 310
• Publication Date: 2016-06
• Subjects: DNA damage and methylation -- epithelial-to-mesenchymal transition -- gastric carcinogenesis -- Helicobacter pylori -- PI3K/Akt; Communicable diseases -- Periodicals; Communicable Diseases -- Periodicals; Review Literature -- Periodicals; 616.905
• DOI: 10.1097/QCO.0000000000000248
• Languages: English
• ISSNs: 0951-7375

Abstract

Abstract : 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.