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Cbfß Reduces Cbfß-SMMHC–Associated Acute Myeloid Leukemia in Mice

¹ Program in Gene Function and Expression, University of Massachusetts Medical School, Worcester, Massachusetts and ² Department of Hematology, Erasmus University Medical Center, Rotterdam, the Netherlands

Requests for reprints: Lucio H. Castilla, Program in Gene Function and Expression, University of Massachusetts Medical School, 364 Plantation Street, LRB/622, Worcester, MA 01605. Phone: 508-856-3281; Fax: 508-856-5460; E-mail: Lucio.Castilla{at}umassmed.edu.

The gene encoding for core-binding factor ß (CBFß) is altered in acute myeloid leukemia samples with an inversion in chromosome 16, expressing the fusion protein CBFß-SMMHC. Previous studies have shown that this oncoprotein interferes with hematopoietic differentiation and proliferation and participates in leukemia development. In this study, we provide evidence that Cbfß modulates the oncogenic function of this fusion protein. We show that Cbfß plays an important role in proliferation of hematopoietic progenitors expressing Cbfß-SMMHC in vitro. In addition, Cbfß-SMMHC–mediated leukemia development is accelerated in the absence of Cbfß. These results indicate that the balance between Cbfß and Cbfß-SMMHC directly affects leukemia development, and suggest that CBF-specific therapeutic molecules should target CBFß-SMMHC function while maintaining CBFß activity. (Cancer Res 2006; 66(23): 11214-8)

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