Pathogenesis of Gastric Cancer. (15th September 2015)

• Record Type: Journal Article
• Authors: Figueiredo, Ceu; Costa, Susana; Karameris, Andreas; Machado, Jose Carlos
• Is Part Of: Helicobacter. Volume 20(2016)Supplement 1
• Page Start: 30
• Page End: 35
• Publication Date: 2015-09-15
• Subjects: Helicobacter pylori -- Epstein–Barr virus -- molecular profiles -- hereditary gastric cancer -- stem cells; Helicobacter -- Periodicals; Helicobacter infections -- Periodicals; Stomach -- Diseases -- Periodicals; 616.3301405
• DOI: 10.1111/hel.12254
• Languages: English
• ISSNs: 1083-4389

Abstract

Abstract : Gastric cancer (GC) is the fifth most common malignancy and the third leading cause of cancer‐related death worldwide. GC is a heterogeneous disease and the endpoint of a long multistep process largely influenced by Helicobacter pylori infection, genetic susceptibility, and environmental factors. In a subset of GC cases, infection with the Epstein–Barr virus (EBV) may also be involved. The development of GC is the consequence of the accumulation of multiple epi/genetic changes during the patient's lifetime that will result in oncogenic activation and/or tumor suppressor pathways' inactivation. This review will focus on the most recent updates on the characterization of the molecular phenotypes of sporadic and hereditary GC. This article will also update the most recent findings on the relationship between H. pylori infection and stem cells at the origin of GC. The understanding of the molecular genetics underlying gastric carcinogenesis is of paramount importance to identify novel potential targets for the development of screening and prognostic markers that can be clinically valuable for the management of GC patients and for the design of clinical trials.