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 Prepublished online as a Blood First Edition Paper on March 6, 2003; DOI 10.1182/blood-2002-10-3182.

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Blood, 1 July 2003, Vol. 102, No. 1, pp. 320-323

NEOPLASIA
Brief report

Myeloproliferative disease in transgenic mice expressing P230 Bcr/Abl: 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

From the Division of Hematology, Department of Internal Medicine, Department of Biochemistry and Molecular Biology, and Research Center for Life Science, Nippon Medical School, Tokyo, Japan; Department of Developmental Biology, Division of Radiation Biology and Medicine, Hiroshima University, Japan; and Department of Hematology/Oncology, Graduate School of Medicine, University of Tokyo, Japan.

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, no. 13, progressed to extramedullary myeloblastic crisis in the liver at 12 months old. The other founder mouse, no. 22, was found to have chronic-phase MPD with large populations of megakaryocytes and granulocytes in an enlarged spleen. The transgenic progeny of no. 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. (Blood. 2003;102:320-323)


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