Intestinal Tumorigenicity of Mice Carrying Hemizygous Pax6, Pax6Sey-4H

DOI Web Site Web Site 被引用文献1件 参考文献18件
  • NITTA Yumiko
    International Radiation Information Center, Research Institute for Radiation Biology and Medicine
  • YOSHIDA Kazuko
    Radiation Hazards Research Group, National Institute for Radiological Science
  • NAKAGATA Naomi
    Center for Animal Resources and Development, Kumamoto University
  • NITTA Kohsaku
    Senogawa Hospital
  • HARADA Toshihide
    Department of Health Services Management, Hiroshima International University
  • ISHIZAKI Fumiko
    Department of Health Science, Hiroshima Prefectural University

この論文をさがす

説明

The genotype-phenotype relationship in mice was examined experimentally using one of the small eye mutants, Pax6Sey-4H, which deletes the chromosome 2 middle region, hemizygously. The genotyping indicated that the deleted region starts at a site 102.60 Mb from the centromere and has a length of 6.51 Mb, in which 12 known and 27 novel genes are located. Expecting the development of myeloid leukemia, gamma-irradiation was performed to female mutants at the age of 10 weeks. The mutants did not develop myeloid leukemia during the observation period of 18 months. Instead, they developed tumors in the alimentary tract spontaneously (56.0%). The tumor latency was shortened by the radiation exposure, but the tumor incidence of the gamma-irradiated group (62.5%) was as high as that of spontaneously developing tumors. Intraductal proliferation of the epithelium of the Wirsung duct was observed in the gamma-irradiated mutants (18.8%). Considering the results of the Pax6Sey-4H mutant together with those of another small eye mutant, Pax6Sey-3H, the anomaly and the tumorigenicity of the intestinal tract were closely related to the hemizygosity of the 3.2 Mb segment of chromosome 2, where both mutants show a common deletion.<br>

収録刊行物

  • Experimental Animals

    Experimental Animals 56 (4), 289-294, 2007

    公益社団法人 日本実験動物学会

被引用文献 (1)*注記

もっと見る

参考文献 (18)*注記

もっと見る

キーワード

詳細情報 詳細情報について

問題の指摘

ページトップへ