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Blood, 19 March 2009, Vol. 113, No. 12, pp. 2795-2804. Prepublished online as a Blood First Edition Paper on January 23, 2009; DOI 10.1182/blood-2008-08-172387. This Article Full Text (PDF) Supplemental Tables and Figures All Versions of this Article: blood-2008-08-172387v1 113/12/2795    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 Figueroa, M. E. Articles by Delwel, R. Search for Related Content PubMed PubMed Citation Articles by Figueroa, M. E. Articles by Delwel, R. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted August 1, 2008 Accepted January 8, 2009 Genome wide epigenetic analysis delineates a biologically distinct immature acute leukemia with myeloid/T-lymphoid features Maria E. Figueroa, Bas J. Wouters, Lucy Skrabanek, Jacob Glass, Yushan Li, Claudia A.J. Erpelinck-Verschueren, Anton W. Langerak, Bob Lowenberg, Melissa Fazzari, John M. Greally, Peter J.M. Valk, Ari Melnick*, and Ruud Delwel Department of Medicine (Hematology Oncology Division), Weill Cornell Medical College, New York, NY, United States Department of Hematology, Erasmus University Medical Center, Rotterdam, Netherlands Department of Physiology and Biophysics, Weill Cornell Medical College, New York, NY, United States Department of Molecular Genetics, Albert Einstein College of Medicine, New York, NY, United States Department of Immunology, Erasmus University Medical Center, Rotterdam, Netherlands Department of Epidemiology and Population Health, Albert Einstein College of Medicine, New York, NY, United States Department of Medicine, Albert Einstein College of Medicine, New York, NY, United States * Corresponding author; email: amm2014{at}med.cornell.edu. Acute Myeloid Leukemia (AML) is a heterogeneous disease from the molecular and biological standpoints, and even patients with a specific gene expression profile may present clinical and molecular heterogeneity. We studied the epigenetic profiles of a cohort of patients that shared a common gene expression profile but differed in that only half of them harbored mutations of the CEBPA locus, while the rest presented with silencing of this gene and aberrant co-expression of certain T cell markers. DNA methylation studies revealed that these two groups of patients could be readily segregated in an unsupervised fashion based on their DNA methylation profiles alone. Furthermore, CEBPA silencing was associated with the presence of an aberrant DNA hypermethylation signature, which was not present in the CEBPA mutant group. This aberrant hypermethylation occurred more frequently at sites within CpG islands. CEBPA silenced leukemias also displayed marked hypermethylation when compared with normal CD34+ hematopoietic cells, while CEBPA mutant cases showed only mild changes in DNA methylation when compared to these normal progenitors. Biologically, CEBPA silenced leukemias presented with a decreased response to myeloid growth factors in vitro. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: T. Pabst and B. U. Mueller Complexity of CEBPA Dysregulation in Human Acute Myeloid Leukemia Clin. Cancer Res., September 1, 2009; 15(17): 5303 - 5307. [Abstract] [Full Text] [PDF] I. H. I. M. Hollink, M. M. van den Heuvel-Eibrink, and C. M. Zwaan CEBPA resembles Roman god Janus Blood, June 25, 2009; 113(26): 6501 - 6502. [Full Text] [PDF]

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