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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 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 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 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. Related Collections Neoplasia Brief Reports Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA Brief Report BCL2 expression in chronic lymphocytic leukemia: lack of association with the BCL2 –938A>C promoter single nucleotide polymorphism Aneela Majid1, Olga Tsoulakis1, Renata Walewska1,2, Stefan Gesk3, Reiner Siebert3, D. Ben J. Kennedy2, and Martin J. S. Dyer1,2 1 Medical Research Council (MRC) Toxicology Unit, Leicester, United Kingdom; 2 Department of Haematology, University Hospitals, Leicester, United Kingdom; 3 Institute of Human Genetics, University Hospital, Schleswig-Holstein, Campus Kiel, Kiel, Germany High-level BCL2 expression is seen in most patients with chronic lymphocytic leukemia (CLL) in the absence of BCL2 chromosomal translocation. A single nucleotide polymorphism (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 patients with CLL for this SNP and 100 patients 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 10 individual patients at different time points. A total of 19 patients with the lowest levels of BCL2 protein expression were biologically and clinically heterogeneous; 5 patients exhibited high-level BCL2 RNA expression and 4 were fludarabine resistant. BCL2 protein levels in CLL reflect a complex interplay of transcriptional and posttranscriptional 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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