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World J Biol Chem. Jun 26, 2011; 2(6): 115-118
Published online Jun 26, 2011. doi: 10.4331/wjbc.v2.i6.115
Up a lymphoid blind alley: Does CALM/AF10 disturb Ikaros during leukemogenesis?
Philipp A Greif, Stefan K Bohlander
Philipp A Greif, Stefan K Bohlander, Clinical Cooperative Group “Leukemia”, Helmholtz Zentrum München, German Research Center for Environmental Health, 81377 Munich, Germany
Philipp A Greif, Stefan K Bohlander, Department of Medicine III, Universität München, 81377 Munich, Germany
Author contributions: Greif PA reviewed the literature and wrote the manuscript; Bohlander SK revised the manuscript.
Correspondence to: Dr. Philipp A Greif, MD, Clinical Cooperative Group “Leukemia”, Helmholtz Zentrum München, German Research Center for Environmental Health, 81377 Munich, Germany. pgreif@med.uni-muenchen.de
Telephone: +49-89-7099410 Fax: +49-89-7099400
Received: March 22, 2011
Revised: May 11, 2011
Accepted: May 18, 2011
Published online: June 26, 2011
Abstract

The Ikaros gene is required for normal development of lymphocytes and frequent intragenic deletions of Ikaros have been identified in acute lymphoblastic leukemia. However, little is known about the role of Ikaros in myeloid malignancies. Here we discuss the role of Ikaros as a lineage master regulator during the onset and progression of myeloid leukemias, namely CALM-AF10 positive acute myeloid leukemia and chronic myeloid leukemia. Alterations of Ikaros at the gene or protein level may act as a bi-directional lineage switch subverting developmental plasticity for malignant transformation. Finally, we propose that promiscuous signaling involving Ikaros and FOXO transcription factors might be a critical link between early lineage fate and uncontrolled proliferation.

Keywords: Acute lymphoblastic leukemia; Acute myeloid leukemia; CALM/AF10; Chronic myeloid leukemia; Ikaros