Published online Nov 21, 2014. doi: 10.3748/wjg.v20.i43.16159
Revised: May 21, 2014
Accepted: June 26, 2014
Published online: November 21, 2014
Processing time: 240 Days and 2.5 Hours
Gastric cancer is the second most frequent cause of cancer death worldwide. Patients infected with Helicobacter pylori (H. pylori) are at increased risk of gastric cancer. H. pylori induces genomic instability in both nuclear and mitochondrial (mt) DNA of gastric epithelial cells. Changes in mtDNA represent an early event during gastric tumorigenesis, and thus may serve as potential biomarkers for early detection and prognosis in gastric carcinoma.This review article summarizes the mtDNA mutations that have been reported in gastric carcinomas and their precancerous conditions. Unexplored research topics, such as the role of mtDNA alterations in an alternative pathway of gastric carcinogenesis, are identified and directions for future research are suggested.
Core tip: Gastric cancer is a heterogeneous disease with multiple environmental etiologies and alternative pathways of carcinogenesis. Somatic mitochondrial DNA (mtDNA) mutations and variable mtDNA copy number are involved in gastric tumorigenesis. The aim of this article is to review the growing literature on the mtDNA changes in gastric carcinomas and in their precancerous conditions. Furthermore, the authors describe which research questions remain unexplored, and suggest future research directions.