Premium
Hepatocarcinogenesis in p53 ‐deficient mice
Author(s) -
Kemp Christopher J.
Publication year - 1995
Publication title -
molecular carcinogenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.254
H-Index - 97
eISSN - 1098-2744
pISSN - 0899-1987
DOI - 10.1002/mc.2940120304
Subject(s) - biology , hepatocellular carcinoma , germline , hepatocellular adenoma , adenoma , malignancy , medicine , wild type , endocrinology , cancer research , mutant , genetics , gene
To determine whether a constitutive p53 deficiency would enhance the rate of development of chemically induced hepatocellular carcinoma, we treated groups of wild‐type, p53 ‐heterozygous (+/‐), and null (‐/‐) male mice with a single dose of diethylnitrosamine at 12 d of age. Although the null mice had to be killed very early, at 15 wk of age because of the development of nonliver tumors, hemangosarcoma of the liver had already developed in two of seven mice. More detailed analysis of the wild‐type and heterozygous mice showed no difference in the number, size, or growth rate of early microscopic lesions or in the number or apparent malignancy of hepatocellular adenomas or carcinomas at later time points. Thus, germline p53 deficiency does not enhance the rate of development of diethylnitrosamine‐induced hepatocellular adenoma or carcinoma but may instead favor development of hepatic hemangiosarcoma. © 1995 Wiley‐Liss Inc.