Inflaming Gastrointestinal Oncogenic Programming

David G. DeNardo, Magnus Johansson, Lisa Coussens

Research output: Contribution to journalArticle

20 Citations (Scopus)

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 TNFα, derived from recruited macrophages, potentiates Wnt/β-catenin signaling and gastric carcinogenesis by activating Akt signaling and GSK3β phosphorylation independent of the NF-κB 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.

Original languageEnglish (US)
Pages (from-to)7-9
Number of pages3
JournalCancer Cell
Volume14
Issue number1
DOIs
StatePublished - Jul 8 2008
Externally publishedYes

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Carcinogenesis
Inflammation
Helicobacter
Catenins
Penetrance
Gastrointestinal Tract
Stomach
Epithelial Cells
Macrophages
Phosphorylation
Mutation
Neoplasms

ASJC Scopus subject areas

  • Cancer Research
  • Cell Biology
  • Oncology

Cite this

Inflaming Gastrointestinal Oncogenic Programming. / DeNardo, David G.; Johansson, Magnus; Coussens, Lisa.

In: Cancer Cell, Vol. 14, No. 1, 08.07.2008, p. 7-9.

Research output: Contribution to journalArticle

DeNardo, David G. ; Johansson, Magnus ; Coussens, Lisa. / Inflaming Gastrointestinal Oncogenic Programming. In: Cancer Cell. 2008 ; Vol. 14, No. 1. pp. 7-9.
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