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Genomic Instability in Chronic Myeloid Leukemia: Targets for Therapy?

  • Chronic Myeloid Leukemia (J Goldman, Section Editor)
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Abstract

Philadelphia positive (Ph+) chronic myeloid leukemia (CML) is characterized by the occurrence of nonrandom genetic and cytogenetic abnormalities during disease progression. Many of these abnormalities are markers for genes which, when altered, can drive the blastic transformation process. Thus, such genetic alterations may be manifestations of an underlying genomic instability resulting from a compromised DNA damage and repair response, leading to advanced stages of CML and resistance to therapy. This article examines the molecular pathways that may lead to genomic instability in CML and the potential of these pathway constituents to be therapeutic targets.

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Acknowledgments

We would like to thank Dr. Kara Scheibner for careful reading of our manuscript. This work was supported by the Valvano Foundation and the Maryland Stem Cell Fund.

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No potential conflicts of interest relevant to this article were reported.

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  1. Department of Radiation Oncology, University of Maryland School of Medicine, 655 West Baltimore Street, Baltimore, MD, 21230, USA

    N. Muvarak, P. Nagaria & F. V. Rassool

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  1. N. Muvarak
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  2. P. Nagaria
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  3. F. V. Rassool
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Correspondence to F. V. Rassool.

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Muvarak, N., Nagaria, P. & Rassool, F.V. Genomic Instability in Chronic Myeloid Leukemia: Targets for Therapy?. Curr Hematol Malig Rep 7, 94–102 (2012). https://doi.org/10.1007/s11899-012-0119-0

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