Molecular Biology of Chronic Myeloid Leukemia

  • Tomasz Sacha
  • Kajetana Foryciarz
  • Aleksander B. Skotnicki
Chapter
Part of the Principles and Practice book series (PRINCIPLES)

Abstract

Chronic myeloid leukemia (CML) is a clonal myeloproliferative disorder resulting from an acquired genetic aberration t(9;22)(q34;q11) (Philadelphia chromosome) in stem cells. As a result the BCR/ABL fusion gene is formed which encodes a specific mRNA, translated into BCR/ABL proteins with an abnormally high tyrosine kinase activity, playing a crucial role in leukemic transformation and neoplastic proliferation of hematopoietic stem cells. BCR/ABL protein activates a number of transcription factors and gene promoters; however, its expression does not explain all the biological mechanisms of the origin of CML and its progression. Trisomy of chromosome 8, 19, isochromosome 17, and an additional Ph chromosome are the most frequent additional chromosomal abnormalities detected in course of CML progression. Suppressor genes dysfunction may play a role in the progression of CML. There is a considerable heterogeneity of the molecular mechanism and the genes involved in the development and progression of CML.

Keywords

Chronic Myeloid Leukemia Chronic Myeloid Leukemia Patient Blast Crisis Blastic Phase Breakpoint Cluster Region 
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.

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Copyright information

© Springer-Verlag Berlin Heidelberg 2012

Authors and Affiliations

  • Tomasz Sacha
    • 1
  • Kajetana Foryciarz
    • 2
  • Aleksander B. Skotnicki
    • 1
  1. 1.Department of HematologyJagiellonian University Hospital in KrakówKrakówPoland
  2. 2.Pharmaceutical Research Associates Sp. z o.o.WarsawPoland

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