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Blood, 1 July 2007, Vol. 110, No. 1, pp. 380-383. Prepublished online as a Blood First Edition Paper on March 14, 2007; DOI 10.1182/blood-2006-12-065599. This Article Full Text Full Text (PDF) Supplemental Table All Versions of this Article: blood-2006-12-065599v1 110/1/380    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 Mohty, M. Articles by Melo, J. V. Search for Related Content PubMed PubMed Citation Articles by Mohty, M. Articles by Melo, J. V. Related Collections Neoplasia Brief Reports Clinical Trials and Observations Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA Brief Report The polycomb group BMI1 gene is a molecular marker for predicting prognosis of chronic myeloid leukemia Mohamad Mohty1, Agnes S. M. Yong1, Richard M. Szydlo1, Jane F. Apperley1, and Junia V. Melo1 1 Department of Hematology, Imperial College London, Hammersmith Hospital, London, United Kingdom Because the polycomb group gene BMI1 regulates the proliferation of both normal and leukemic stem cells, we examined whether BMI1 expression was associated with disease progression in chronic myeloid leukemia (CML). Levels of BMI1 RNA were significantly higher in patients with advanced-phase than in patients with chronic-phase CML in both CD34+ cells (P = .006) and total peripheral-blood mononuclear cells (P < .001). E2F1, a transcription factor regulating BMI1, was up-regulated in CML compared with controls (P = .001). In a cohort of 64 CML patients, the level of BMI1 at diagnosis correlated with time to transformation to blast crisis, and the combination of low BMI1 and high proteinase-3 expression was associated in multivariate analysis with an improved overall survival (P = .001). We conclude that BMI1 may be a biomarker for the intrinsic heterogeneity of CML, and its measurement at diagnosis can help predict overall survival and thus contribute to better therapeutic decisions. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: A. Rizo, S. Olthof, L. Han, E. Vellenga, G. de Haan, and J. J. Schuringa Repression of BMI1 in normal and leukemic human CD34+ cells impairs self-renewal and induces apoptosis Blood, August 20, 2009; 114(8): 1498 - 1505. [Abstract] [Full Text] [PDF] M. Mohty, R. M. Szydlo, A. S. M. Yong, J. F. Apperley, J. M. Goldman, and J. V. Melo Association between BMI-1 expression, acute graft-versus-host disease, and outcome following allogeneic stem cell transplantation from HLA-identical siblings in chronic myeloid leukemia Blood, September 1, 2008; 112(5): 2163 - 2166. [Abstract] [Full Text] [PDF] E. Kavalerchik, D. Goff, and C. H.M. Jamieson Chronic Myeloid Leukemia Stem Cells J. Clin. Oncol., June 10, 2008; 26(17): 2911 - 2915. [Abstract] [Full Text] [PDF] A. Rizo, B. Dontje, E. Vellenga, G. de Haan, and J. J. Schuringa Long-term maintenance of human hematopoietic stem/progenitor cells by expression of BMI1 Blood, March 1, 2008; 111(5): 2621 - 2630. [Abstract] [Full Text] [PDF] C. H. Jamieson Chronic Myeloid Leukemia Stem Cells Hematology, January 1, 2008; 2008(1): 436 - 442. [Abstract] [Full Text] [PDF] K. Dorshkind and O. N. Witte Linking the hematopoietic microenvironment to imatinib-resistant Ph+ B-ALL Genes & Dev., September 15, 2007; 21(18): 2249 - 2252. [Full Text] [PDF]

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