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Receptor Tyrosine Kinase Alterations in AML – Biology and Therapy

  • Derek L. Stirewalt
  • Soheil Meshinchi
Chapter
Part of the Cancer Treatment and Research book series (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.

Keywords

Acute Myeloid Leukemia Small Molecule Inhibitor Acute Myeloid Leukemia Patient Acute Myeloid Leukemia Cell Internal Tandem Duplication 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Notes

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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© Springer Science+Business Media, LLC 2009

Authors and Affiliations

  1. 1.Clinical Research DivisionFrom Fred Hutchinson Cancer Research CenterSeattleUSA

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