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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. This Article Full Text Full Text (PDF) All Versions of this Article: 2003-12-4111v1 103/11/4010    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Calabretta, B. Articles by Perrotti, D. Search for Related Content PubMed PubMed Citation Articles by Calabretta, B. Articles by Perrotti, D. Related Collections Cell Cycle Oncogenes and Tumor Suppressors Signal Transduction Gene Expression Reviews in Translational Hematology Neoplasia Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  The biology of CML blast crisis Bruno Calabretta, and Danilo Perrotti From the Department of Microbiology and Immunology, Kimmel Cancer Center, Thomas Jefferson Medical College, Philadelphia, PA; Department of Biomedical Sciences, University of Modena, Italy; and Human Cancer Genetics Program, Department of Molecular Virology, Immunology, and Medical Genetics and the Comprehensive Cancer Center, Ohio State University, Columbus. Abstract 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 chromosomal 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 genes dysregulated during disease progression. Most genetic abnormalities of CML blast crisis have a direct or indirect effect on p53 or Rb (or both) 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 (ie, C/EBP). Validation of the critical role of certain secondary changes (ie, 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 (ie, p53 or C/EBP). CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: C. G. Mullighan, R. T. Williams, J. R. Downing, and C. J. Sherr Failure of CDKN2A/B (INK4A/B-ARF)-mediated tumor suppression and resistance to targeted therapy in acute lymphoblastic leukemia induced by BCR-ABL Genes & Dev., June 1, 2008; 22(11): 1411 - 1415. [Abstract] [Full Text] [PDF] A. Pierce, R. D. Unwin, C. A. Evans, S. Griffiths, L. Carney, L. Zhang, E. Jaworska, C.-F. Lee, D. Blinco, M. J. Okoniewski, et al. 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