Host: The Japan Radiation Research Society, Chairman of the 52nd Annual Meeting, Toshiteru Okubo (Radiation Effects Research Foundation)
Min mouse is susceptible to radiation tumorigenesis. The efficacy depends on the age at exposure, with a peak at 1-2 weeks of age. Exposure at 7 weeks of age has little enhancement. To better understand the molecular mechanism in the age-dependent radiation tumorigenesis, we carried out detailed LOH analysis of chromosome 18 to which the Apc gene maps, by using statistical method for LOH detection in the tumors of chromosome 18 consomic-Min mice. LOH profiling of the chromosome 18 revealed a difference between the small intestine and the colon, as well as spontaneous and radiation-induced tumors. A majority of spontaneous tumors exhibited MSM allele loss spanning wide range or entire chromosome 18, while tumors induced by 2-week-old exposure exhibited LOH restricted to specific narrow regions, a region spanning the Apc gene, distal chromosome 18, and proximal chromosome 18. Lost allele was of MSM origin (normal allele) in the Apc gene, and of both origins in the distal and proximal chromosome 18. There is a tendency that distal and proximal chromosome 18 had lost alleles of the same origin.
