Epidermal growth factor receptor inhibition downregulates Helicobacter pylori-induced epithelial inflammatory responses, DNA damage and gastric carcinogenesis.

ABSTRACT:

Objective

Gastric cancer is the third leading cause of cancer death worldwide and infection by Helicobacter pylori is the strongest risk factor. We have reported increased epidermal growth factor receptor (EGFR) phosphorylation in the H. pylori-induced human carcinogenesis cascade, and association with DNA damage. Our goal was to determine the role of EGFR activation in gastric carcinogenesis.

Design

We evaluated gefitinib, a specific EGFR inhibitor, in chemoprevention of H. pylori-induced gastric inflammation and cancer development. Mice with genetically targeted epithelial cell-specific deletion of Egfr (Efgr^Δepi mice) were also used.

Results

In C57BL/6 mice, gefitinib decreased Cxcl1 and Cxcl2 expre

SUBMITTER: Sierra JC 

PROVIDER: S-EPMC5671361 | biostudies-literature | 2018 Jul

REPOSITORIES: biostudies-literature