Related Experiment Video
Updated: Jul 3, 2026

Multi-Gene Single Nucleotide Polymorphism Detection in Gastric Cancer Based on Ion Semiconductor Sequencing Platform
Published on: May 10, 2024
Inflaming gastrointestinal oncogenic programming
David G DeNardo1, Magnus Johansson, Lisa M Coussens
1Department of Pathology, University of California, San Francisco, San Francisco, CA 94143, USA.
Abstract:
The etiology of gastrointestinal tumors implicates a role for chronic inflammation in response to pathogenic microflora as a promoting force for full neoplastic progression. Recently, Oguma and coworkers (2008) demonstrated that TNFalpha, derived from recruited macrophages, potentiates Wnt/beta-catenin signaling and gastric carcinogenesis by activating Akt signaling and GSK3beta phosphorylation independent of the NF-kappaB pathway in initiated epithelial cells. These observations provide a missing link in the mechanism whereby chronic inflammation, in response to Helicobacter, regulates the "penetrance" of initiating oncogenic mutations in the gastrointestinal tract leading to gastrointestinal tumorigenesis.
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