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Vol. 13, No. 10, pp. 1240-1245, May 15, 1999
1 Department of Immunology, 2 Department of
Surgical Oncology, and 4 Department of Pathology, Graduate
School of Medicine and Faculty of Medicine, University of Tokyo,
Bunkyo-ku, Tokyo 113-0033, Japan; 3 Department of DNA Biology
and Embryo Engineering, Institute of Medical Science, University of
Tokyo, Minato-ku, Tokyo 108-8639, Japan; 5 Central Institute
for Experimental Animals, Miyamae-ku, Kawasaki, Kanagawa 216-0001, Japan; 6 Institute of Molecular Embryology and Genetics,
Faculty of Medicine, Kumamoto University, Kumamoto 860-0811, Japan
The transcription factor IRF-1 has been implicated in tumor
suppression: IRF-1 suppresses cell transformation and mediates apoptosis in vitro. Here we show that the loss of IRF-1 alleles per se has no effect on spontaneous tumor development in the mouse but
dramatically exacerbates previous tumor predispositions caused by the
c-Ha-ras transgene or by nullizygosity for p53. Grossly altered tumor spectrum, as compared to p53-null mice, was also observed in mice lacking both IRF-1 and p53, and cells
from these mice show significantly higher mutation rate. Our results
suggest that IRF-1 is a new member of the tumor susceptibility genes.
[Key Words: IRF-1; c-Ha-ras; p53; tumor susceptibility gene; mutation frequency]
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