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Prepublished online as a Blood First Edition Paper on March 6, 2003; DOI 10.1182/blood-2002-10-3182. This Article Full Text (PDF) All Versions of this Article: 2002-10-3182v1 102/1/320    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Inokuchi, K. Articles by Shimada, T. Search for Related Content PubMed PubMed Citation Articles by Inokuchi, K. Articles by Shimada, T. Social Bookmarking                   What's this? Submitted October 22, 2002 Accepted February 21, 2003 Novel transgenic mice expressing P230 Bcr/Abl developed myeloproliferative disorder: longer disease latency, thrombocytosis, and mild leukocytosis Koiti Inokuchi*, Kazuo Dan, Miyuki Takatori, Hidemasa Takahuji, Naoya Uchida, Mitsuharu Inami, Koichi Miyake, Hiroaki Honda, Hisamaru Hirai, and Takashi Shimada Division of Hematology, Department of Internal Medicine, Nippon Medical School, Tokyo, Japan Research Center for Life Science, Nippon Medical School, Tokyo, Japan Department of Biochemistry and Molecular Biology, Nippon Medical School, Tokyo, Japan Department of Developmental Biology, Division of Radiation Biology and Medicine, Hiroshima University, Hiroshima, Japan Department of Hematology/Oncology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan * Corresponding author; email: inokuchi{at}nms.ac.jp. P230 Bcr/Abl has been associated with indolent myeloproliferative disease (MPD). We generated transgenic mice expressing P230Bcr/Abl driven by the promoter of the long terminal repeat of the murine stem cell virus of the MSCV neo P230 BCR/ABL vector. Two founder mice exhibited mild granulocytosis and marked thrombocytosis and developed MPD. The disease of one founder mouse, #13, progressed to extramedullary myeloblastic crisis in the liver at 12 months old. The other founder mouse, #22, was found to have chronic-phase MPD with large populations of megakaryocytes and granulocytes in an enlarged spleen. The transgenic progeny of #22 clearly exhibited MPD at 15 months old. These results showed that P230Bcr/Abl had leukemogenic properties and induced MPD. The phenotype of the MPD caused by P230Bcr/Abl was characterized by mild granulocytosis, a high platelet count, infiltration of megakaryocytes in some organs, and a longer disease latency compared with the MPD caused by P210Bcr/Abl. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: B C Mondal, S Majumdar, U B Dasgupta, U Chaudhuri, P Chakrabarti, and S Bhattacharyya e19a2 BCR-ABL fusion transcript in typical chronic myeloid leukaemia: a report of two cases. J. Clin. Pathol., October 1, 2006; 59(10): 1102 - 1103. [Abstract] [Full Text] [PDF]

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