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
Pages (from-to)7-9
Number of pages3
JournalCancer Cell
Issue number1
StatePublished - Jul 8 2008


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