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 Blood, 1 April 2005, Vol. 105, No. 7, pp. 2900-2907.
Prepublished online as a Blood First Edition Paper on December 7, 2004; DOI 10.1182/blood-2004-09-3630.

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NEOPLASIA

Plag1 and Plagl2 are oncogenes that induce acute myeloid leukemia in cooperation with Cbfb-MYH11

Sean F. Landrette, Ya-Huei Kuo, Karen Hensen, Sahar Barjesteh van Waalwijk van Doorn-Khosrovani, Paola N. Perrat, Wim J. M. Van de Ven, Ruud Delwel, and Lucio H. Castilla

From the Program in Gene Function and Expression, University of Massachusetts Medical School, Worcester, MA; the Laboratory for Molecular Oncology, Center for Human Genetics (CME), University of Leuven (KUL), Leuven, Belgium; and The Institute for Hematology, Erasmus Medical Center, Rotterdam, The Netherlands.

Recurrent chromosomal rearrangements are associated with the development of acute myeloid leukemia (AML). The frequent inversion of chromosome 16 creates the CBFB-MYH11 fusion gene that encodes the fusion protein CBF{beta}-SMMHC. This fusion protein inhibits the core-binding factor (CBF), resulting in a block of hematopoietic differentiation, and induces leukemia upon the acquisition of additional mutations. A recent genetic screen identified Plag1 and Plagl2 as CBF{beta}-SMMHC candidate cooperating proteins. In this study, we demonstrate that Plag1 and Plagl2 independently cooperate with CBF{beta}-SMMHC in vivo to efficiently trigger leukemia with short latency in the mouse. In addition, Plag1 and Plagl2 increased proliferation by inducing G1 to S transition that resulted in the expansion of hematopoietic progenitors and increased cell renewal in vitro. Finally, PLAG1 and PLAGL2 expression was increased in 20% of human AML samples. Interestingly, PLAGL2 was preferentially increased in samples with chromosome 16 inversion, suggesting that PLAG1 and PLAGL2 may also contribute to human AML. Overall, this study shows that Plag1 and Plagl2 are novel leukemia oncogenes that act by expanding hematopoietic progenitors expressing CbF{beta}-SMMHC.


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