[Recent progress in molecular biology of chemically-induced hepatic carcinogenesis].
Chemically-induced hepatic carcinogenesis is a suitable model to investigate multistep process of carcinogenesis, because preneoplastic and neoplastic lesions develop in a sequential manner. The process is initiated by emergency of "genetically altered cells" or "initiated cells" which have a potential to progress to hepatocellular carcinomas. The cells can clonally expand under the effect of tumor promoters or carcinogens. Clonal expansion will increase the probability that a cell undergoes further genetic changes. By this stepwise manner, a cell may acquire neoplastic properties such as independence to growth factors, invasive growth, loss of antigenicity, metastatic capacity, etc. The author reviewed the recent advance in studies on oncogenes, tumor suppressor genes and growth factor genes concerning to rodent hepatic carcinogenesis.
Ogawa
K
K
Department of Pathology, Asahikawa Medical College.
D000818:Animals; D004052:Diethylnitrosamine; D016259:Genes, myc; D016158:Genes, p53; D011905:Genes, ras; D006801:Humans; D007335:Insulin-Like Growth Factor II / Q000378:metabolism; D008114:Liver Neoplasms, Experimental / Q000139:chemically induced* / Q000235:genetics / Q000473:pathology; D051379:Mice; D017354:Point Mutation; D051381:Rats; D016211:Transforming Growth Factor alpha / Q000378:metabolism
D016211:Transforming Growth Factor alpha; D004052:Diethylnitrosamine; D007335:Insulin-Like Growth Factor II