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Blood, 15 January 2008, Vol. 111, No. 2, pp. 874-877. Prepublished online as a Blood First Edition Paper on October 24, 2007; DOI 10.1182/blood-2007-07-098681. This Article Full Text (PDF) Supplemental Methods, Table, and Figures All Versions of this Article: blood-2007-07-098681v1 111/2/874    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 Majid, A. Articles by Dyer, M. J.S. Search for Related Content PubMed PubMed Citation Articles by Majid, A. Articles by Dyer, M. J.S. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted July 2, 2007 Accepted October 11, 2007 BCL2 expression in chronic lymphocytic leukemia (CLL): lack of association with the BCL2 -938A>C promoter single nucleotide polymorphism (SNP) Aneela Majid, Olga Tsoulakis, Renata Walewska, Stefan Gesk, Reiner Siebert, D. Ben J. Kennedy, and Martin J.S. Dyer* Department of Hematology, MRC Toxicology Unit, Leicester, United Kingdom Institute of Human Genetics, University Hospital, Schleswig-Holstein, Campus Kiel, Kiel, Germany Department of Hematology, University Hospitals Leicester, Leicester, United Kingdom * Corresponding author; email: mjsd1{at}le.ac.uk. High-level BCL2 expression is seen in most cases of CLL in the absence of BCL2 chromosomal translocation. A SNP (-938C>A) within an inhibitory region of the BCL2 promoter has been reported to regulate BCL2 protein expression and to be associated with adverse prognostic features in CLL. We screened 276 cases of CLL for this SNP and 100 cases by quantitative western blot for BCL2 expression. In contrast to the previous report, we found no association with BCL2 protein levels or with any clinical or laboratory parameters. BCL2 protein levels remained constant in ten individual cases at different time points. 19 cases showing the lowest levels of BCL2 protein expression were biologically and clinically heterogeneous. Five cases exhibited high-level BCL2 RNA expression and four were fludarabine-resistant. BCL2 protein levels in CLL reflect a complex interplay of transcriptional and post-transcriptional controls, but do not appear to be associated with the -938C>A promoter SNP. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: D. Ishimaru, S. Ramalingam, T. K. Sengupta, S. Bandyopadhyay, S. Dellis, B. G. Tholanikunnel, D. J. Fernandes, and E. K. Spicer Regulation of Bcl-2 Expression by HuR in HL60 Leukemia Cells and A431 Carcinoma Cells Mol. Cancer Res., August 1, 2009; 7(8): 1354 - 1366. [Abstract] [Full Text] [PDF] M. Vogler, M. Butterworth, A. Majid, R. J. Walewska, X.-M. Sun, M. J. S. Dyer, and G. M. Cohen Concurrent up-regulation of BCL-XL and BCL2A1 induces approximately 1000-fold resistance to ABT-737 in chronic lymphocytic leukemia Blood, April 30, 2009; 113(18): 4403 - 4413. [Abstract] [Full Text] [PDF]

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