BCR–ABL1 lymphoblastic leukaemia is characterized by the deletion of Ikaros

Charles G. Mullighan, Christopher B. Miller, Ina Radtke, Letha A. Phillips, James Dalton, Jing Ma, Deborah White, Timothy P. Hughes, Michelle M. Le Beau, Ching-Hon Pui, Mary V. Relling, Sheila A. Shurtleff and James R. Downing ()
Additional contact information
Charles G. Mullighan: Departments of Pathology,
Christopher B. Miller: Departments of Pathology,
Ina Radtke: Departments of Pathology,
Letha A. Phillips: Departments of Pathology,
James Dalton: Departments of Pathology,
Jing Ma: The Hartwell Center for Bioinformatics and Biotechnology, St Jude Children’s Research Hospital, Memphis, Tennessee 38105, USA
Deborah White: The Institute for Medical and Veterinary Science, Adelaide, South Australia 5000, Australia
Timothy P. Hughes: The Institute for Medical and Veterinary Science, Adelaide, South Australia 5000, Australia
Michelle M. Le Beau: Section of Hematology/Oncology, University of Chicago, Chicago, Illinois 60637, USA
Ching-Hon Pui: Oncology and,
Mary V. Relling: Pharmaceutical Sciences and,
Sheila A. Shurtleff: Departments of Pathology,
James R. Downing: Departments of Pathology,

Nature, 2008, vol. 453, issue 7191, 110-114

Abstract: Ikaros protein in ALL The Philadelphia chromosome is a genetic abnormality associated with chronic myelogenous leukaemia and some types of acute lymphoblastic leukaemia. It produces an abnormal signalling protein causing bone marrow cells to multiply uncontrollably. Now Mullighan et al. identify another mutant protein that contributes to this destructive process. Over 80% of a group of acute lymphoblastic leukaemia patients with the Philadelphia chromosome also lacked the gene IKZF1. The protein encoded by this gene is Ikaros, a lymphoid cell-specific transcription factor. The loss of Ikaros activity seems to cause a crucial malfunctioning that can contribute to the development of acute lymphoblastic leukaemia in the presence of the Philadelphia lesion.

Date: 2008
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DOI: 10.1038/nature06866

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