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Prepublished online as a Blood First Edition Paper on February 13, 2003; DOI 10.1182/blood-2002-09-2906. This Article Full Text Full Text (PDF) All Versions of this Article: 2002-09-2906v1 101/12/4903    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 McCarthy, H. Articles by Abruzzo, L. V. Search for Related Content PubMed PubMed Citation Articles by McCarthy, H. Articles by Abruzzo, L. V. Related Collections Immunobiology Neoplasia Oncogenes and Tumor Suppressors Gene Expression Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 15 June 2003, Vol. 101, No. 12, pp. 4903-4908 IMMUNOBIOLOGY High expression of activation-induced cytidine deaminase (AID) and splice variants is a distinctive feature of poor-prognosis chronic lymphocytic leukemia Helen McCarthy, William G. Wierda, Lynn L. Barron, Candy C. Cromwell, Jing Wang, Kevin R. Coombes, Roberto Rangel, Kojo S. J. Elenitoba-Johnson, Michael J. Keating, and Lynne V. Abruzzo From the Departments of Leukemia, Hematopathology, Biostatistics, and Immunology, The University of Texas M. D. Anderson Cancer Center, Houston, TX; and the Division of Anatomic Pathology, University of Utah Health Sciences Center, Salt Lake City, UT. In chronic lymphocytic leukemia (CLL), analysis of immunoglobulin heavy chain variable regions for somatic hypermutation identifies 2 prognostic subsets, mutated and unmutated. Investigators have postulated that unmutated and mutated CLL arises from malignant transformation of pre– and post–germinal center (GC) B cells, respectively. Alternatively, unmutated cases may arise from B cells stimulated by T-cell–independent antigens or from GC B cells with inactive somatic hypermutation. Activation-induced cytidine deaminase (AID), a protein essential for somatic hypermutation, is expressed by GC B cells in which this process occurs. We investigated AID mRNA expression in 20 CLL cases. In 8 cases we detected high expression of wild-type AID mRNA and 2 splice variants; in 12 cases and 5 normal peripheral blood B-cell samples we detected no expression using standard conditions. Of 8 CLL cases that highly expressed AID, 7 were unmutated, suggesting that this subset may arise from GC-experienced B cells with inactive somatic hypermutation, and may predict prognosis. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: K. J. McCann, M. Ashton-Key, K. Smith, F. K. Stevenson, and C. H. Ottensmeier Primary central nervous system lymphoma: tumor-related clones exist in the blood and bone marrow with evidence for separate development Blood, May 7, 2009; 113(19): 4677 - 4680. [Abstract] [Full Text] [PDF] X. Wu, J. R. Darce, S. K. Chang, G. S. Nowakowski, and D. F. Jelinek Alternative splicing regulates activation-induced cytidine deaminase (AID): implications for suppression of AID mutagenic activity in normal and malignant B cells Blood, December 1, 2008; 112(12): 4675 - 4682. [Abstract] [Full Text] [PDF] A. 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