Pharmacological activation of epidermal growth factor receptor signaling inhibits colitis-associated cancer in mice.

ABSTRACT: Current treatments for inflammatory bowel disease (IBD) target the overactive immune response of the intestinal mucosa. However, epidermal growth factor (EGF), an activating ligand of the EGF receptor (EGFR), has been shown to induce disease remission through direct targeting of intestinal mucosal healing. Despite promising preclinical and clinical results, this EGFR-activating therapy has not progressed, in part due to the potential for carcinogenesis associated with long-term use and the increased risk of colitis-associated cancer (CAC) in IBD. Here we tested whether pharmacological modulation of EGFR altered outcomes of CAC in the murine azoxymethane/dextran sulfate sodium model. We found that administering EGF during the period of maximum colitis severity ("early"), coincident with the

SUBMITTER: Dube PE 

PROVIDER: S-EPMC6002410 | biostudies-literature | 2018 Jun

REPOSITORIES: biostudies-literature