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p53 mutations are absent from carcinogen‐induced mouse liver tumors but occur in cell lines established from these tumors
Author(s) -
Kress Stefan,
König Jorg,
Schweizer Jürgen,
Löhrke Heinz,
BauerHofmann Richard,
Schwarz Michael
Publication year - 1992
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.2940060210
Subject(s) - biology , point mutation , gene , carcinogen , microbiology and biotechnology , allele , mutation , cell culture , cancer research , liver tumor , carcinogenesis , in vitro , gene mutation , genetics , hepatocellular carcinoma
Mutations in the p53 gene are frequent genetic alterations in human hepatocellular carcinomas We have examined, by single‐strand conformation polymorphism analysis of polymerase chain reaction products, a total of 93 carcinogen‐induced liver tumors from mice of three different strains (C3H/He, C57BL/6J, and B6C3F1) for the presence of p53 aberrations. Hepatoma lines, established from 12 liver tumors, were also included in the analysis. While structural aberrations of the p53 gene were not detected in any of the primary mouse liver tumors analyzed, single‐base substitutions occurred at different locations within the p53 gene in three of the cell lines during in vitro propagation. One hepatoma line carried two point mutations on separate alleles. All four mutations were either G:C→C:G or C:G→G:C transversions. Mutations at codon 61 of the c‐Ha‐ ras gene, which were frequent in primary liver tumors from C3H/He and B6C3F1 mice, were not detected in the hepatoma lines. Our data indicate (i) that c‐Ha‐ ras but not p53 mutations play an important role during the early stages of mouse hepatocarcinogenesis and (ii) that p53 mutations confer a selective growth advantage to the mutated hepatoma cells in vitro. © 1992 Wiley‐Liss, Inc.