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Blood, 1 June 2004, Vol. 103, No. 11, pp. 4010-4022.
Prepublished online as a Blood First Edition Paper on February 24, 2004; DOI 10.1182/blood-2003-12-4111.
Submitted December 2, 2003
Accepted February 5, 2004
The Biology of CML Blast Crisis
Bruno Calabretta* and Danilo Perrotti
Microbiology, Kimmel Cancer Center, Philadelphia, PA, none
Molecular Virology, Immunology and Medical Genetics, The Ohio State University, Columbus, OH, none
* Corresponding author; email: b_calabretta{at}lac.jci.tju.edu.
Chronic myelogenous leukemia (CML) evolves from a chronic phase characterized by the Philadelphia chromosome as the sole genetic abnormality into blast crisis, which is often associated with additional genetic and molecular secondary changes. Although the pathogenic effects of most CML blast crisis secondary changes are still poorly understood, ample evidence suggests that the phenotype of CML blast crisis cells (enhanced proliferation and survival, differentiation arrest) depends on cooperation of BCR/ABL with gene(s) dysregulated during disease progression. Most genetic abnormalities of CML blast crisis have a direct or indirect effect on p53 and/or Rb gene activity which are primarily required for cell proliferation and survival, but not differentiation. Thus, the differentiation arrest of CML blast crisis cells is a secondary consequence of these abnormalities or is caused by dysregulation of differentiation-regulatory genes (i.e. C/EBP ) Validation of the critical role of certain secondary changes (i.e. loss of p53 or C/EBP function) in murine models of CML blast crisis and in in vitro assays of BCR/ABL transformation of human hematopoietic progenitors might lead to the development of novel therapies based on targeting BCR/ABL and inhibiting or restoring the gene activity gained or lost during disease progression (i.e. p53 or C/EBP).
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