Host: The Japan Radiation Research Society
Co-host: Asian Association for Radiation Research
To elucidate the molecular mechanism in radiation tumorigenesis in mice, we generated a mouse strain by substituting an entire chromosome18 in B6-Min mouse. The consomic-Min mouse strain is highly susceptible to radiation tumorigenesis; mice exposed to 2.0 Gy of X-rays at 2 weeks of age induced 7-fold small intestinal tumors and 29-fold colonic tumors over the unirradiated mice. The enhancement was dependent on the age at exposure; mice exposed at 7 weeks of age had lost the susceptibility to the radiation tumorigenesis. LOH analysis at the Apc locus revealed that radiation-induced colonic tumors showed significantly higher LOH frequency compared to the spontaneous tumors. Detailed LOH analysis using 24 SSLP markers on the chromosome 18 revealed that the vast majority of the radiation-induced intestinal tumors exhibited intra-chromosomal recombination, while spontaneous tumors showed entire loss of the chromosome 18 without any sign of the recombination. In all the cases mentioned above, normal allele of the Apc gene had been lost. Possible chromosome region where frequent recombination had occurred in the radiaton-induced tumors was suggested.
