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The BALB/c-IL10 null mouse strain develops colitis and colitis-associated adenocarcinomas, and is a model for idiopathic inflammatory bowel disease. We tested the hypotheses that (i) azoxymethane (AOM), a carcinogen that targets the colon, synergizes with the colonic inflammation inherent in the BALB/c-IL10 null mouse resulting in an increase in incidence, multiplicity and/or progression of AOM-induced tumors or colitis-associated adenocarcinomas; and (ii) prior infection withHelicobacter hepaticus, a common enterohepatic bacterial pathogen in many research mouse colonies, increases the incidence, multiplicity and/or progression of AOM-induced colon tumors or colitis-associated adenocarcinomas in the BALB/c-IL10 null mouse. We show that, within the timeframe examined, AOM-induced colon tumors in the BALB/c-IL10 null mouse were grossly and microscopically similar in appearance to AOM-induced colon tumors in the wild type BALB/cJ mouse. No colitis-associated adenocarcinomas were identified. Infection withH. hepaticusprior to AOM-treatment also did not result in colitis-associated adenocarcinomas but did result in a significant increase in the incidence of AOM-induced colon tumors relative to AOM treatment alone. The AOM-induced adenomas were predominantly exophytic and nodular or polypoid and localized to the distal colon. These results suggest thatH. hepaticuspromotes AOM-induced tumorigenesis in the BALB/c-IL10 null mouse.