Tumor necrosis factor-α polymorphism in helicobacter pylori associated gastric carcinoma

Background: Gastric cancer (GC) is the leading cause of cancer death in the world. Chronic inflammation is a predisposing factor of gastric carcinogenesis. TNF-α is a key pro-inflammatory cytokine secreted by macrophages and causes development of malignant diseases. It also plays an important role i...

Full description

Saved in:
Bibliographic Details
Published in:Bangladesh Medical Research Council bulletin Vol. 45; no. 3; pp. 170 - 174
Main Authors: Barua, Rita Rani, Barua, Sushanta, Barua, Hena Rani, Barua, Ajoy Kishore, Ansari, M.A. Jalil, Chong, J-M, Uozaki, Hiroshi, Fukayama, Masashi
Format: Journal Article
Language:English
Published: 30-12-2019
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Background: Gastric cancer (GC) is the leading cause of cancer death in the world. Chronic inflammation is a predisposing factor of gastric carcinogenesis. TNF-α is a key pro-inflammatory cytokine secreted by macrophages and causes development of malignant diseases. It also plays an important role in chronic inflammation caused by Helicobacter Pylori. Therefore, TNF-α polymorphisms is studied in Helicobacter Pylori infected gastric cancer. Objective: To find out the high risk group of Helicobacter Pylori infected gastric cancer cases in Asian and Caucasian people. Methods: A total of 130 GC cases and 103 healthy controls from Jichi Medical School, Japan were studied. TNF-α genotype and allele frequency were studied by Restriction Fragment Length Polymorphism (RFLP). Results: Among the study population TNFa-308A was less frequent in Asian people than those of Caucasian. TNFa-238G allele was more frequent in H. pylori positive GC (p<0.036) cases. Conclusion: Findings of the study suggest that TNF-238G polymorphism of TNF-α gene may be closely associated with susceptibility to Helicobacter Pylori infected gastric cancer in Asian patients.  This might be due to high cytokine production by TNF-238G allele.
ISSN:0377-9238
2224-7238
DOI:10.3329/bmrcb.v45i3.44647