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Blood, 12 March 2009, Vol. 113, No. 11, pp. 2517-2525. Prepublished online as a Blood First Edition Paper on January 13, 2009; DOI 10.1182/blood-2008-07-169110. This Article Full Text Full Text (PDF) Supplemental Tables and Figure All Versions of this Article: blood-2008-07-169110v1 113/11/2517    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 CrossRef Citing Articles via Google Scholar Google Scholar Articles by Kim, D. H. Articles by Lipton, J. H. Search for Related Content PubMed PubMed Citation Articles by Kim, D. H. Articles by Lipton, J. H. Related Collections Myeloid Neoplasia Clinical Trials and Observations Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  MYELOID NEOPLASIA Genetic variants in the candidate genes of the apoptosis pathway and susceptibility to chronic myeloid leukemia Dong Hwan (Dennis) Kim1,2,*, Wei Xu3,*, Clement Ma3, Xiangdong Liu4, Katherine Siminovitch4, Hans A. Messner1, and Jeffrey H. Lipton1 1 Chronic Myelogenous Leukemia Group, Department of Hematology/Medical Oncology, Princess Margaret Hospital, University Health Network, University of Toronto, Toronto, ON; 2 Department of Hematology/Oncology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea; 3 Department of Biostatistics, Princess Margaret Hospital, University Health Network, University of Toronto, Toronto, ON; and 4 Analytical Genetics Technology Centre, University Health Network, Toronto, ON Chronic myeloid leukemia (CML) is a clonal myeloproliferative disorder, characterized by the presence of BCR/ABL fusion gene. It is unclear which cellular events drive BCR/ABL gene translocation or initiate leukemogenesis in CML. Bcl-2 promotes survival of hematopoietic stem cells. Accordingly, apoptosis-related pathway may involve in the leukemogenesis of CML. In the current study, we evaluated 80 single nucleotide polymorphism (SNP) markers involved in the pathways of apoptosis (n = 30), angiogenesis (n = 7), myeloid cell growth (n = 14), xenobiotic metabolism (n = 13), WT1 signaling (n = 7), interferon signaling (n = 4), and others (n = 5) in 170 CML patients and 182 healthy controls. In a single-marker analysis, the following SNPs were identified including VEGFA, BCL2, CASP7, JAK3, CSF3, and HOCT1. In the multivariate logistic model with these SNPs and covariates, only BCL2 (rs1801018) was significantly associated with the susceptibility to CML (P = .05; odds ratio [OR] 2.16 [1.00-4.68]). In haplotype analyses, haplotype block of BCL2 consistently showed significant association with the susceptibility to CML. Risk allele analysis showed that a greater number of risk alleles from BCL2 SNP correlated to increasing risk of CML (overall P = .1, OR 1.84 [1.06-3.22] for 3-4 risk alleles vs 0-1 risk alleles). The current study indicated that BCL2 SNP seemed to be associated with increasing susceptibility to CML. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

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