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Spontaneous liver tumors and Benzo[a]pyrene‐induced lymphomas in XPA‐deficient mice
Author(s) -
de Vries Annemieke,
van Oostrom Conny T. M.,
Dortant Paul M.,
Beems Rudolf B.,
van Kreijl Coen F.,
Capel Peter J. A.,
van Steeg Harry
Publication year - 1997
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/(sici)1098-2744(199705)19:1<46::aid-mc7>3.0.co;2-l
Subject(s) - xeroderma pigmentosum , biology , nucleotide excision repair , cancer research , carcinogen , photodermatosis , skin cancer , complementation , microbiology and biotechnology , carcinogenesis , cancer , gene , dna repair , genetics , mutant
Defects in the xeroderma pigmentosum complementation group A‐correcting (XPA) gene, which encodes a component of the nucleotide excision repair (NER) pathway, are associated with the cancer‐prone human disease xeroderma pigmentosum. We previously generated mice lacking the XPA gene, which develop normally but are highly sensitive to ultraviolet‐B and 7,12‐dimethylbenz[a]anthracene‐induced skin tumors. Here we report the XPA‐deficient mice spontaneously developed hepatocellular adenomas at a low frequency as they aged. Furthermore, oral treatment of XPA‐deficient mice with the carcinogen benzo[a]pyrene (B[a]P) resulted in the induction of mainly lymphomas. These tumors appeared earlier and with a higher incidence than in B[a]P‐treated wild‐type and heterozygous mice. Our results show for the first time that XPA‐deficient mice also displayed an increased sensitivity to developing tumors other than tumors of the skin. Mol. Carcinog. 19:46–53, 1997. © 1997 Wiley‐Liss, Inc.