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 Blood, 1 February 2007, Vol. 109, No. 3, pp. 1237-1240.
Prepublished online as a Blood First Edition Paper on September 28, 2006; DOI 10.1182/blood-2006-07-037465.

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NEOPLASIA

Brief Report

Expression of a bcr-1 isoform of RAR{alpha}-PML does not affect the penetrance of acute promyelocytic leukemia or the acquisition of an interstitial deletion on mouse chromosome 2

Matthew J. Walter1,2,3, Rhonda E. Ries1,2, Jon R. Armstrong4, John S. Park1,2, Elaine R. Mardis4, and Timothy J. Ley1,2,3

1 Department of Medicine, 2 Division of Oncology, 3 Siteman Cancer Center, and 4 Genome Sequencing Center, Washington University School of Medicine, St Louis, MO

Expression of a bcr-3 isoform of retinoic acid receptor {alpha}–promyelocytic leukemia (RAR{alpha}-PML) in mice expressing a bcr-1 isoform of PML-RAR{alpha} is associated with increased penetrance of murine acute promyelocytic leukemia (APL) and the frequent acquisition of an interstitial deletion of one copy of mouse chromosome 2 (del(2)). To determine whether the isoform of RAR{alpha}-PML is important for these effects, we created mice that expressed a bcr-1 isoform of RAR{alpha}-PML. Coexpression with the bcr-1 isoform of PML-RAR{alpha} did not increase the penetrance of APL (7 of 45 animals developed APL with PML-RAR{alpha} alone vs 12 of 44 with both transgenes; P = .19). Furthermore, the frequency of del(2) in APL cells from doubly transgenic mice was not different from that of mice expressing PML-RAR{alpha} alone (3 of 6 vs 6 of 12, respectively—P = 1.38—compared with 11 of 11 for mice coexpressing PML-RAR{alpha} and bcr-3 RAR{alpha}-PML). The bcr-1 and bcr-3 isoforms of RAR{alpha}-PML, therefore, have different biological activities that may be relevant for the pathogenesis of murine APL.


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