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Receptor Tyrosine Kinase Alterations in AML – Biology and Therapy

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Acute Myelogenous Leukemia

Part of the book series: Cancer Treatment and Research ((CTAR,volume 145))

Abstract

Acute myeloid leukemia (AML) is the most common form of leukemia in adults, and despite some recent progress in understanding the biology of the disease, AML remains the leading cause of leukemia-related deaths in adults and children. AML is a complex and heterogeneous disease, often involving multiple genetic defects that promote leukemic transformation and drug resistance. The cooperativity model suggests that an initial genetic event leads to maturational arrest in a myeloid progenitor cell, and subsequent genetic events induce proliferation and block apoptosis. Together, these genetic abnormalities lead to clonal expansion and frank leukemia. The purpose of this chapter is to review the biology of receptor tyrosine kinases (RTKs) in AML, exploring how RTKs are being used as novel prognostic factors and potential therapeutic targets.

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Acknowledgments

Support for the authors was provided by National Institutes of Health grants (K23 CA92405 and CA 114563). This work was supported by National Institute of Health grants no. K23 CA92405-01 and CA18029.

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  1. Clinical Research Division, From Fred Hutchinson Cancer Research Center, Seattle, WA, USA

    Derek L. Stirewalt & Soheil Meshinchi MD, PhD

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  1. Dept. of Genetics, MD Anderson Cancer Center, Holcombe Blvd. 1515, Houston, 77030, USA

    Lalitha Nagarajan

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Stirewalt, D.L., Meshinchi, S. (2009). Receptor Tyrosine Kinase Alterations in AML – Biology and Therapy. In: Nagarajan, L. (eds) Acute Myelogenous Leukemia. Cancer Treatment and Research, vol 145. Springer, New York, NY. https://doi.org/10.1007/978-0-387-69259-3_6

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