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[Cancer Research 63, 902-905, March 1, 2003]
© 2003 American Association for Cancer Research

Advances in Brief

Ogg1 Knockout-associated Lung Tumorigenesis and Its Suppression by Mth1 Gene Disruption1

Kunihiko Sakumi2, Yohei Tominaga, Masato Furuichi, Ping Xu, Teruhisa Tsuzuki, Mutsuo Sekiguchi and Yusaku Nakabeppu

Division of Neurofunctional Genomics, Medical Institute of Bioregulation, Kyushu University and CREST, JST, Fukuoka 812-8582 [K. S., Y. T., M. F., P. X., Y. N.]; Department of Medical Biophysics and Radiation Biology, Graduate School of Medical Science, Kyushu University, Fukuoka 812-8582 [T. T.]; and Biomolecular Engineering Research Institute, Suita 565-0874 [M. S.], Japan

Using Mth1 and Ogg1 knockout mice, we evaluated the roles of these enzymes to prevent tumorigenesis and the accumulation of 8-oxoguanine (8-oxoG) in DNA. We found that lung adenoma/carcinoma spontaneously developed in Ogg1 knockout mice ~1.5 years after birth in which 8-oxoG was found to accumulate in their genomes. The mean number of tumors/mouse was 0.71 for the Ogg1 knockout mice, which was five times higher than that observed in wild-type mice (0.14). Although the accumulation of 8-oxoG was also confirmed in the Ogg1, Mth1 double knockout mice, we found no tumor in the lungs of these mice. This observation suggests that Mth1 gene disruption resulted in a suppression of the tumorigenesis caused by an Ogg1 deficiency.




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