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Carcinogenesis, Vol. 23, No. 4, 627-633, April 2002
© 2002 Oxford University Press

CARCINOGENESIS

Enhanced spontaneous and aflatoxin-induced liver tumorigenesis in xeroderma pigmentosum group A gene-deficient mice

Yoshihisa Takahashi1, Yoko Nakatsuru1, Shaomin Zhang1, Yasuhito Shimizu1, Haruki Kume1, Kiyoji Tanaka2, Fumio Ide1 and Takatoshi Ishikawa3,4

1 Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, Tokyo 113-0033,
2 Institute for Molecular and Cellular Biology, Osaka University, 1–3 Yamadaoka, Suita, Osaka 565-0871 and
3 National Institution for Academic Degrees, Faculty of University Evaluation and Research, 2-1-2 Hitotsubashi, Chiyoda-ku, Tokyo 101-0003, Japan

Xeroderma pigmentosum (XP) is an autosomal recessive hereditary disease featuring defective nucleotide excision repair (NER). XP patients are highly sensitive to sunlight and develop skin cancer at an early age. While the fact that XP patients have a large increase in mortality from skin cancers has been extensively documented, the relation between XP and internal tumors has received little attention. We therefore analyzed development of spontaneous and aflatoxin B1 (AFB1)-induced liver tumors in XPA-deficient congenic mice, originally created by repeated back-crosses with inbred C3H/HeN mice. Spontaneous liver tumors were assessed at the age of 16 months in two separate experiments using F5 and F10 lines. The incidence of and average number of spontaneous tumors per mouse were significantly higher in XPA-/- than in XPA+/+ and +/- mice. Similarly, F10 XPA-/- mice receiving i.p. injection of 0.6 or 1.5 mg/kg b.w. AFB1 at 7 days of age demonstrated more liver tumors than their heterozygous or homozygous positive counterparts when examined at month 11. These results demonstrate that XPA-deficient mice have increased susceptibility to both spontaneous liver tumor development and AFB1-induced hepatocarcinogenesis.


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