Modification of early dimethylhydrazine carcinogenesis by colonic mucosal hyperplasia.
The interaction of colonic mucosal hyperplasia with early 1,2-dimethylhydrazine (DMH) carcinogenesis was studied in random-bred NIH Swiss mice utilizing hyperplasia-inducing Citrobacter freundii. Mice inoculated with this bacterium developed significantly more DMH focal atypia than did mice without hyperplasia following a single dose of DMH (20 mg/kg). Mice with hyperplasia also developed DMH focal atypia with diminished doses of DMH (10 and 5 mg/kg), while normal mice did not. The effect of C. freundii on early DMH carcinogenesis was shown to be due to the hyperplasia rather than to a direct interaction of the bacterium with DMH. Focal atypia arose in high incidence 1 month after a single dose of DMH (20 mg/kg) but did not appear to progress to later stages of neoplasia, since significantly fewer atypia were present at 2 to 4 months among a randomized population. Colonic focal atypia may represent a reversible preneoplastic or precursor lesion as seen in other tissues, with features more aligned to neoplasia than to hyperplasia.
D000818:Animals; D002954:Citrobacter; D003043:Cocarcinogenesis; D003110:Colonic Neoplasms / Q000209:etiology*; D004127:Dimethylhydrazines; D004756:Enterobacteriaceae Infections / Q000150:complications; D006965:Hyperplasia / Q000150:complications*; D007413:Intestinal Mucosa / Q000473:pathology*; D008763:Methylhydrazines; D051379:Mice; D009374:Neoplasms, Experimental / Q000209:etiology
D004127:Dimethylhydrazines; D008763:Methylhydrazines