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Volume 271, Number 38, Issue of September 20, 1996 pp. 22976-22982
©1996 by The American Society for Biochemistry and Molecular Biology, Inc.

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Deregulated Expression of c-myc in Megakaryocytes of Transgenic Mice Increases Megakaryopoiesis and Decreases Polyploidization

(Received for publication, January 25, 1996, and in revised form, May 31, 1996)

Alexander Thompson , Ying Zhang , Dimitry Kamen , Carl W. Jackson ^§ , Robert D. Cardiff ^¶ and Katya Ravid

From the  Department of Biochemistry, Boston University School of Medicine, Boston, Massachusetts 02139, the ^§ Division of Experimental Hematology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, and the ^¶ Department of Medical Pathology, University of California at Davis, Sacramento, California 95817

Platelets, essential for vascular integrity and hemostasis, fragment from polyploid megakaryocytes, characterized by their endomitotic cell cycle. We studied the influence of overexpression of c-myc oncogene on megakaryopoiesis and endomitosis in vivo, using transgenic mice carrying c-myc fused to the estrogen receptor under the control of the platelet factor 4 (PF4) megakaryocyte-specific promoter. The rationale behind this strategy was to obtain controlled overexpression of an active c-Myc, depending on the estrogen level in the mouse circulation. Analysis of these transgenic mice revealed that the bone marrow of female transgenic mice or of estrogen-injected male transgenic mice, but not of age-matched transgenic males nor nontransgenic females, contained frequent immature myeloid cells and an increased number of megakaryocytes. Deregulated expression of c-Myc shifted the normal ploidy profile of megakaryocytes due to a significant increase in proliferating megakaryocytes and a decrease in the fraction of ploidizing cells. These transgenic mice represent a novel in vivo model for a Myc-induced myeloproliferative disorder which can be controlled.

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