Published online Nov 21, 2018. doi: 10.3748/wjg.v24.i43.4928
Peer-review started: June 8, 2018
First decision: July 4, 2018
Revised: September 11, 2018
Accepted: October 5, 2018
Article in press: October 5, 2018
Published online: November 21, 2018
Processing time: 166 Days and 10.1 Hours
Gastric cancer (GC) is the world’s fourth leading cause of cancer deaths, and microbial infections have been shown to contribute to gastric tumorigenesis.
Gastric physiology and immunology are known to be altered by Helicobacter pylori (H. pylori) and Epstein-Barr virus (EBV), although there is still doubt about the association of GC with some pathogens, such as human papillomavirus (HPV).
The present study aimed to elucidate the possible relationship of these microorganisms with the clinical-pathological characteristics of patients with GC in the North region of Brazil.
A total of 302 gastric adenocarcinomas were collected between 2005 and 2015. Patient samples were categorized according to the TNM classification system and by histology. Molecular techniques were used for pathogen investigations, as they are more sensitive.
All three pathogens were found in the samples; however, active HPV infection was not identified. Coinfections of H. pylori-cagA+ and EBV were correlated with tumors at the most advanced stages.
HPV was not involved in gastric tumorigenesis. On the other hand, H. pylori and EBV seem to be directly related to the development and severity of tumors, especially when coinfections exist.
Prophylactic and therapeutic measures against H. pylori and EBV may prevent the development of GC, especially the more aggressive forms.