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Prepublished online as a Blood First Edition Paper on May 13, 2002; DOI 10.1182/blood-2001-11-0026. This Article Full Text Full Text (PDF) All Versions of this Article: 2001-11-0026v1 100/7/2572    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 Li, Y. Articles by Kinoshita, T. Search for Related Content PubMed PubMed Citation Articles by Li, Y. Articles by Kinoshita, T. Related Collections Cell Cycle Oncogenes and Tumor Suppressors Gene Expression Neoplasia Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 1 October 2002, Vol. 100, No. 7, pp. 2572-2577 NEOPLASIA Aberrant DNA methylation of p57KIP2 gene in the promoter region in lymphoid malignancies of B-cell phenotype Yinghua Li, Hirokazu Nagai, Toshihito Ohno, Masaaki Yuge, Sonoko Hatano, Etsuro Ito, Naoyoshi Mori, Hidehiko Saito, and Tomohiro Kinoshita From the First Department of Internal Medicine, and the First Department of Pathology, Nagoya University School of Medicine; the Department of Hematology, Nagoya National Hospital; and the Aichi Blood Disease Research Foundation, Nagoya, Japan; and from the Department of Pediatrics, School of Medicine, Hirosaki University, Japan. The cyclin-dependent kinase inhibitor p57KIP2 is thought to be a potential tumor suppressor gene (TSG). The present study examines this possibility. We found that the expression of p57KIP2 gene is absent in various hematological cell lines. Exposing cell lines to the DNA demethylating agent 5-aza-2'-deoxycytidine restored p57KIP2 gene expression. Bisulfite sequencing analysis of its promoter region showed that p57KIP2 DNA was completely methylated in cell lines that did not express the p57KIP2 gene. Thus, DNA methylation of its promoter might lead to inactivation of the p57KIP2 gene. DNA methylation of this region is thought to be an aberrant alteration, since DNA was not methylated in normal peripheral blood mononuclear cells or in reactive lymphadenitis. Methylation-specific polymerase chain reaction analysis found frequent DNA methylation of the p57KIP2 gene in primary diffuse large B-cell lymphoma (54.9%) and in follicular lymphoma (44.0%), but methylation was infrequent in myelodysplastic syndrome and adult T-cell leukemia (3.0% and 2.0%, respectively). These findings directly indicate that the profile of the p57KIP2 gene corresponds to that of a TSG. © 2002 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: V. Cucciolla, A. Borriello, M. Criscuolo, A. A. Sinisi, D. Bencivenga, A. Tramontano, A. C. Scudieri, A. Oliva, V. Zappia, and F. D. Ragione Histone deacetylase inhibitors upregulate p57Kip2 level by enhancing its expression through Sp1 transcription factor Carcinogenesis, March 1, 2008; 29(3): 560 - 567. [Abstract] [Full Text] [PDF] H. Shi, J. Guo, D. J. Duff, F. Rahmatpanah, R. Chitima-Matsiga, M. Al-Kuhlani, K. H. Taylor, O. Sjahputera, M. Andreski, J. E. Wooldridge, et al. Discovery of novel epigenetic markers in non-Hodgkin's lymphoma Carcinogenesis, January 1, 2007; 28(1): 60 - 70. 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