イワサキ　マサユキ   Iwasaki Masayuki   岩崎　正幸    所属   研究施設 研究施設    職種   講師
論文種別	原著
言語種別	英語
査読の有無	査読あり
表題	Haploinsufficiency of Runx1/AML1 promotes myeloid features and leukaemogenesis in BXH2 mice.
掲載誌名	正式名：British journal of haematology 略　 称：Br J Haematol ISSNコード：00071048/00071048
掲載区分	国外
巻・号・頁	131(4),pp.495-507
著者・共著者	Yamashita Namiko, Osato Motomi, Huang Liqun, Yanagida Masatoshi, Kogan Scott C, Iwasaki Masayuki, Nakamura Takuro, Shigesada Katsuya, Asou Norio, Ito Yoshiaki
発行年月	2005/11
概要	Haploinsufficiency of RUNX1/AML1 is associated with familial platelet disorder with a predisposition to acute myeloid leukaemia (FPD/AML), but the causal relationship remains to be addressed experimentally. Mice heterozygous for the Runx1 null mutation, Runx1+/-, are considered to be genetically comparable with human FPD/AML patients but do not develop spontaneous leukaemia. To induce additional genetic alterations, retroviral insertional mutagenesis was employed with the use of BXH2 mice, which develop myeloid leukaemia because of the random integration of retrovirus present in the mouse. Heterozygous disruption of Runx1 in BXH2 mice resulted in a shortening of the latency period of leukaemia. In addition, BXH2-Runx1+/- mice exhibited more marked myeloid features than control mice. Moreover, the c-Kit gene, mutated in human RUNX leukaemias, was recurrently activated in BXH2-Runx1+/- mice, and a colony-forming assay revealed synergism between the Runx1+/- status and c-KIT overexpression. In conclusion, the BXH2-Runx1+/- system is a promising mouse model to investigate the mechanism of leukaemogenesis in FPD/AML.
DOI	10.1111/j.1365-2141.2005.05793.x
PMID	16281942