The role of necrosis in hepatocellular proliferation and liver tumors.
A sequence of events which appear to be common in the development of cancer in all mammalian species includes atrophy, hyperplasia, and neoplasia. Evidence to date suggests that cell death (necrosis) is an integral, perhaps essential, factor in the initiation and maintenance of the process but the extent to which necrosis is involved, and the nature of that participation is unclear. Choline deficient B6C3F1 mice have been used to accentuate and investigate necrosis and the development of liver neoplasia following exposure to aflatoxin B1. The binding of AFB1 to DNA correlates with the level of acute necrosis and the early appearance of foci of alteration and later, tumor development. Adducts of GSH-DNA varied as do other parameters including products of peroxidation, but the relation of these variables to necrosis and cancer are unclear at present. These parameters are currently under study.
D016604:Aflatoxin B1; D000348:Aflatoxins; D000818:Animals; D001549:Benzamides; D002277:Carcinoma / Q000139:chemically induced / Q000473:pathology; D002796:Choline Deficiency; D006965:Hyperplasia; D008099:Liver / Q000473:pathology*; D008114:Liver Neoplasms, Experimental / Q000139:chemically induced / Q000473:pathology*; D008297:Male; D051379:Mice; D008809:Mice, Inbred C3H; D008810:Mice, Inbred C57BL; D009336:Necrosis; D051381:Rats; D011919:Rats, Inbred Strains; D012643:Selenium
D000348:Aflatoxins; D001549:Benzamides; C001059:pronamide; D016604:Aflatoxin B1; D012643:Selenium