SEARCH:   Advanced

Blood, 19 February 2009, Vol. 113, No. 8, pp. 1619-1630. Prepublished online as a Blood First Edition Paper on September 30, 2008; DOI 10.1182/blood-2008-03-144790. This Article Full Text (PDF) All Versions of this Article: blood-2008-03-144790v1 113/8/1619    most recent Alert me when this article is cited Alert me if a correction is posted 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 Quintas-Cardama, A. Articles by Cortes, J. Search for Related Content PubMed PubMed Citation Articles by Quintas-Cardama, A. Articles by Cortes, J. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted March 13, 2008 Accepted August 20, 2008 Molecular biology of BCR-ABL1-positive chronic myeloid leukemia Alfonso Quintas-Cardama* and Jorge Cortes Department of Leukemia, The University of Texas M.D. Anderson Cancer Center, Houston, TX, United States * Corresponding author; email: aquintas{at}mdanderson.org. Chronic myelogenous leukemia (CML) has been regarded as the paradigmatic example of a malignancy defined by a unique molecular event, the BCR-ABL1 oncogene. Decades of research zeroing in on the role of BCR-ABL1 kinase in the pathogenesis of CML have culminated in the development of highly efficacious therapeutics which, like imatinib mesylate, target the oncogenic kinase activity of BCR-ABL1. In recent years, most research efforts in CML have been devoted to developing novel tyrosine kinase inhibitors (TKIs) as well as to elucidating the mechanisms of resistance to imatinib and other TKIs. Yet, primordial aspects of the pathogenesis of CML such as the mechanisms responsible for the transition from chronic phase to blast crisis, the causes of genomic instability and faulty DNA repair, the phenomenon of stem cell quiescence, the role of tumor suppressors in TKI resistance and CML progression, or the cross-talk between BCR-ABL1 and other oncogenic signaling pathways still remain poorly understood. Herein, we synthesize the most relevant and current knowledge on such areas of the pathogenesis of CML. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: N. Testoni, G. Marzocchi, S. Luatti, M. Amabile, C. Baldazzi, M. Stacchini, M. Nanni, G. Rege-Cambrin, E. Giugliano, U. Giussani, et al. Chronic myeloid leukemia: a prospective comparison of interphase fluorescence in situ hybridization and chromosome banding analysis for the definition of complete cytogenetic response: a study of the GIMEMA CML WP Blood, December 3, 2009; 114(24): 4939 - 4943. [Abstract] [Full Text] [PDF] G. Rosti, F. Palandri, F. Castagnetti, M. Breccia, L. Levato, G. Gugliotta, A. Capucci, M. Cedrone, C. Fava, T. Intermesoli, et al. Nilotinib for the frontline treatment of Ph+ chronic myeloid leukemia Blood, December 3, 2009; 114(24): 4933 - 4938. [Abstract] [Full Text] [PDF] D. Verma, H. M. Kantarjian, D. Jones, R. Luthra, G. Borthakur, S. Verstovsek, M. B. Rios, and J. Cortes Chronic myeloid leukemia (CML) with P190BCR-ABL: analysis of characteristics, outcomes, and prognostic significance Blood, September 10, 2009; 114(11): 2232 - 2235. [Abstract] [Full Text] [PDF]

	Copyright © 2008 by American Society of Hematology         Online ISSN: 1528-0020