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

Matthew J. Walter, Rhonda E. Ries, Jon R. Armstrong, John S. Park, Elaine R. Mardis, Timothy J. Ley

Research output: Contribution to journalArticle

7 Scopus citations

Abstract

Expression of a bcr-3 isoform of retinoic acid receptor α-promyelocytic leukemia (RARα-PML) in mice expressing a bcr-1 isoform of PML-RARα 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 RARα-PML is important for these effects, we created mice that expressed a bcr-1 isoform of RARα-PML. Coexpression with the bcr-1 isoform of PML-RARα did not increase the penetrance of APL (7 of 45 animals developed APL with PML-RARα 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-RARα alone (3 of 6 vs 6 of 12, respectively - P = 1.38 - compared with 11 of 11 for mice coexpressing PML-RARα and bcr-3 RARα-PML). The bcr-1 and bcr-3 isoforms of RARα-PML, therefore, have different biological activities that may be relevant for the pathogenesis of murine APL.

Original languageEnglish
Pages (from-to)1237-1240
Number of pages4
JournalBlood
Volume109
Issue number3
DOIs
StatePublished - Feb 1 2007

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