Overexpression of β–catenin and EphB4 in Helicobacter pylori infected Mexican children with gastritis

Abstract

Chronic inflammation and infection are major gastric carcinogenic risk factors. As Helicobacter pylori (HP) infection is common in children, determining if HP infection is an early event in gastric carcinogenesis identifies a potential therapeutic target for reducing gastric cancer (GC) in these patients. Gastritis activity, atrophy, follicular pathology (FP), intestinal metaplasia (IM) and expression of 9 biomarkers (Ephrin Type‐B Receptor 4 [EphB4], Activation‐Induced Cytidine Deaminase, Caudal Type Homeobox 2 [Cdx2], p53, Macrophage Migration Inhibitory Factor, Matrix Metalloproteinase 3, α‐Methylacyl‐CoA Racemase, β‐catenin, Ecadherin) involved in gastric carcinogenesis and progression were examined in antral biopsies from 36 HP+ and 46HP‐ Mexican children (mean age 8.1y) with chronic gastritis. EphB4 expression (p=0.008), β‐catenin staining intensity (p=0.002), activity, atrophy and FP (p=0.0002, p<0.0001 and p=0.0007) significantly correlated with HP+ biopsies. 6 children (3 HP+) demonstrated aberrant Cdx2 expression without histological evidence of IM. Antral biopsies demonstrating preneoplastic markers may identify high risk patients who would benefit from anti‐HP therapy and closer follow up surveillance. R.V.C. recognizes generous support from FASEB and ASIP Minority Access to Research Careers Summer Research Opportunities Program in Pathology.