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This Article Full Text Full Text (PDF) 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 Rush, L. J. Articles by Plass, C. Search for Related Content PubMed PubMed Citation Articles by Rush, L. J. Articles by Plass, C. Related Collections Neoplasia Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 15 May 2001, Vol. 97, No. 10, pp. 3226-3233 NEOPLASIA Novel methylation targets in de novo acute myeloid leukemia with prevalence of chromosome 11 loci Laura J. Rush, Zunyan Dai, Dominic J. Smiraglia, Xin Gao, Fred A. Wright, Michael Frühwald, Joseph F. Costello, William A. Held, Li Yu, Ralf Krahe, Jonathan E. Kolitz, Clara D. Bloomfield, Michael A. Caligiuri, and Christoph Plass From the Division of Human Cancer Genetics, Department of Molecular Virology, Immunology and Medical Genetics; the Department of Veterinary Biosciences; the Department of Pathology; the Division of Hematology and Oncology, Department of Internal Medicine; and the Comprehensive Cancer Center, The Ohio State University, Columbus; the Ludwig Institute for Cancer Research, University of California-San Diego, La Jolla; the Department of Molecular and Cellular Biology, Roswell Park Cancer Institute, New York, and the Don Monti Division of Medical Oncology and Division of Hematology, North Shore University Hospital, Manhasset, NY; and the Cancer and Leukemia Group B, Chicago IL. Aberrant DNA methylation is believed to be important in tumorigenesis by causing either transcriptional inactivation of genes or chromosomal instability. Several laboratories have identified promoter hypermethylation of tumor suppressor genes in acute myeloid leukemia (AML). However, these studies do not provide a global assessment of overall methylation changes and do not allow the identification of novel methylated sequences. Previously, nonrandom CpG island methylation was reported in 17 adult de novo AML diagnostic samples when compared with the corresponding remission samples by means of restriction landmark genomic scanning (RLGS). That study has been expanded on by an analysis of a larger set of CpG islands (1740 vs 1184), which now provides details of 33 cloned methylated loci, including 21 known genes or expressed sequence tags. Five of these cloned loci appear to be methylated only in AML and not in the 6 solid tumors studied in this study (more than 98 samples analyzed). Chromosomal location was available for 30 of the 33 loci, and 5 of these 30 (17%) are localized to chromosome 11, suggesting a trend toward overrepresentation of methylation events on this chromosome. These results provide evidence for widespread aberrant methylation in AML, with identification of novel methylation targets, epigenetic changes that appear unique to AML, and apparent preferential methylation on chromosome 11. © 2001 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: B. Hackanson, K. L. Bennett, R. M. Brena, J. Jiang, R. Claus, S.-S. Chen, N. Blagitko-Dorfs, K. Maharry, S. P. Whitman, T. D. Schmittgen, et al. Epigenetic Modification of CCAAT/Enhancer Binding Protein {alpha} Expression in Acute Myeloid Leukemia Cancer Res., May 1, 2008; 68(9): 3142 - 3151. [Abstract] [Full Text] [PDF] C. Hong, K. S. Moorefield, P. Jun, K. D. Aldape, S. Kharbanda, H. S. 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