Oncogene-induced liver neoplasia in transgenic mice.

摘要: Models of hepatocarcinogenesis were generated by directing the expression SV40 T-antigens, an oncogenic mutant c-H-ras, or c-myc to liver transgenic mice using albumin enhancer/promoter. The majority carrying ras transgene (group A) born with enlarged livers and atypical hepatic architecture, these all died within several days birth. remaining B) had lower levels expression, exhibited mild dysplasia but no enlargement, ultimately from development lung tumors. In contrast, expressing T-antigens relatively normal at birth, one month displayed marked dysplasia, three seven months developed multiple nodular adenomas carcinomas. Myc caused severe in young mice, focal some over fifteen age. Lines B), T-antigen, myc established crossed each other generate dual oncogene pairs. Each combination resulted accelerated tumor development, suggesting that oncoproteins can cooperate another during multistep transformation.