@article{oai:repo.qst.go.jp:00043459,
 author = {Nitta, Yumiko and Yoshida, Kazuko and et.al and 新田 由美子 and 吉田 和子},
 journal = {Journal of Toxicologic Pathology},
 month = {},
 note = {Allelic loss of chromosome 2 is associated with radiation-induced murine acute myeloid leukemia. However, the gene, which contributes mainly to the leukemogenesis in a tumor suppression manner, has not been identified, yet. Expecting predisposition to acute myeloid leukemia, a radiation leukemogenesis experiment was performed with Pax6Sey3H, one of the small mutants. Deletion mapping of Pax6Sey3H indicated that the deleted segment extended from 106.00 to 111.47 Mb from the centromere with a length of 5.47 Mb on chromosome 2. Six known and seventeen novel genes were located in the segment. Pax6Sey3H mutants crossed back into C3H/He did not develop hematopoietic tumors spontaneously, but they did after exposure to gamma rays. The final incidence of hematopoietic tumor in mutants (45.2%) was higher than that in normal sibs (26.2%), and the survival curve of mutants shifted toward the left (p less than 0.05 by the Cox-Mantel test). Mutants developed intestinal tumors spontaneously with long latency as well as showing abnormality in the Wirsung s duct from young ages. Congenital deletion of the 5.47 Mb segment at the middle region on chromosome 2 alone did not trigger hematopoietic tumors, however, the deletion promoted the development of hematopoietic tumors initiated by radiation. The deletion developed intestinal tumors spontaneously. Radiation exposure at 10 weeks of age did not contribute to the intestinal tumorigenesis.},
 pages = {105--112},
 title = {Effects of a Hemizygous Deletion of Mouse Chromosome 2 on the Hematopoietic and Intestinal Tumorigenesis},
 volume = {17},
 year = {2004}
}