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(American Journal of Pathology. 2003;163:1729-1733.)
© 2003 American Society for Investigative Pathology

Short Communication

p53 Haploinsufficiency Profoundly Accelerates the Onset of Tongue Tumors in Mice Lacking the Xeroderma Pigmentosum Group A Gene

Fumio Ide*, Munenori Kitada{dagger}, Hideaki Sakashita{dagger}, Kaoru Kusama*, Kiyoji Tanaka{ddagger} and Takatoshi Ishikawa§

From the Department of Oral Pathology* and the Second Department of Oral and Maxillofacial Surgery,{dagger} Meikai University School of Dentistry, Saitama, Japan; the Division of Cellular Genetics,{ddagger} Institute of Molecular and Cellular Biology, Osaka University, Osaka, Japan; and the Second Department of Pathology,§ Graduate School of Medicine, University of Tokyo, Tokyo, Japan

Mice lacking the xeroderma pigmentosum group A gene (XPA-/- mice), which have a complete deficiency in nucleotide excision repair (NER), are highly predisposed to tongue squamous cell carcinoma (SCC) when exposed to 4-nitroquinoline 1-oxide (4NQO). To explore the effects of the interaction of the NER machinery with p53 in oral tumorigenesis, we generated an XPA-/- mouse strain carrying mutant alleles for p53. This mouse model of 4NQO carcinogenesis demonstrated that despite the same tumor frequency, XPA-/-p53+/- mice reached 100% SCC incidence at 25 weeks compared with 50 weeks for XPA-/-p53+/+ littermates. XPA-/-p53-/- mice succumbed to spontaneous thymic lymphomas before the development of tongue tumors (before 13 weeks of age). SCC originated in XPA-/-p53+/- mice maintained the p53+/- genotype and the retained wild-type p53 allele appeared to be structurally intact. Only one of 20 XPA-/-p53+/+ SCC showed a missense mutation of p53. Collectively, the accelerated tongue tumor growth may be a consequence of haploinsufficiency but not of mutation of p53 in the context of NER deficiency.




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