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      Is Open Access

      Association of variants in BAFF (rs9514828 and rs1041569) and BAFF-R (rs61756766) genes with the risk of chronic lymphocytic leukemia

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          Abstract

          The B-cell activator factor (BAFF)/BAFF receptor (BAFF-R) axis seems to play an important role in the development and progression of chronic lymphocytic leukemia (CLL). Here, we investigated the association of eight single nucleotide polymorphisms (SNPs) in the BAFF (TNFSF13B) and BAFF-R (TNFRSF13C) genes with risk of sporadic CLL in a group of 439 CLL patients and 477 controls. We also examined the correlation between selected SNPs and CLL clinical parameters as well as BAFF plasma levels and intracellular BAFF expression. Our results point to a possible association between the rs9514828 (CT vs. CC + TT; OR = 0.74; CI 95 % = 0.57; 0.97; p = 0.022) and rs1041569 (AT vs. AA + TT; OR = 0.72; CI 95 % = 0.54; 0.95; p = 0.021) of BAFF gene and rs61756766 (CC vs. CT; OR = 2.03; CI 95 % = 1.03; 3.99; p = 0.03) of BAFF-R gene and CLL risk. Additionally, we observed that homozygotes rs1041569 AA and TT had a slightly higher risk (HR = 1.12) for the need of treatment in comparison to AT heterozygotes. In conclusion, our results indicate that SNPs in BAFF and BAFF-R genes may be considered as potential CLL risk factors.

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          The online version of this article (doi:10.1007/s13277-016-5182-z) contains supplementary material, which is available to authorized users.

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          Maximum-likelihood estimation of molecular haplotype frequencies in a diploid population.

          L Excoffier, M Slatkin (1995)
          Molecular techniques allow the survey of a large number of linked polymorphic loci in random samples from diploid populations. However, the gametic phase of haplotypes is usually unknown when diploid individuals are heterozygous at more than one locus. To overcome this difficulty, we implement an expectation-maximization (EM) algorithm leading to maximum-likelihood estimates of molecular haplotype frequencies under the assumption of Hardy-Weinberg proportions. The performance of the algorithm is evaluated for simulated data representing both DNA sequences and highly polymorphic loci with different levels of recombination. As expected, the EM algorithm is found to perform best for large samples, regardless of recombination rates among loci. To ensure finding the global maximum likelihood estimate, the EM algorithm should be started from several initial conditions. The present approach appears to be useful for the analysis of nuclear DNA sequences or highly variable loci. Although the algorithm, in principle, can accommodate an arbitrary number of loci, there are practical limitations because the computing time grows exponentially with the number of polymorphic loci. Although the algorithm, in principle, can accommodate an arbitrary number of loci, there are practical limitations because the computing time grows exponentially with the number of polymorphic loci.
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            Alternatives to the Median Absolute Deviation

            Peter Rousseeuw, Christophe Croux (1993)
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              Sp1 and the 'hallmarks of cancer'.

              Kate Beishline, Jane Azizkhan-Clifford (2015)
              For many years, transcription factor Sp1 was viewed as a basal transcription factor and relegated to a role in the regulation of so-called housekeeping genes. Identification of Sp1's role in recruiting the general transcription machinery in the absence of a TATA box increased its importance in gene regulation, particularly in light of recent estimates that the majority of mammalian genes lack a TATA box. In this review, we briefly consider the history of Sp1, the founding member of the Sp family of transcription factors. We review the evidence suggesting that Sp1 is highly regulated by post-translational modifications that positively and negatively affect the activity of Sp1 on a wide array of genes. Sp1 is over-expressed in many cancers and is associated with poor prognosis. Targeting Sp1 in cancer treatment has been suggested; however, our review of the literature on the role of Sp1 in the regulation of genes that contribute to the 'hallmarks of cancer' illustrates the extreme complexity of Sp1 functions. Sp1 both activates and suppresses the expression of a number of essential oncogenes and tumor suppressors, as well as genes involved in essential cellular functions, including proliferation, differentiation, the DNA damage response, apoptosis, senescence and angiogenesis. Sp1 is also implicated in inflammation and genomic instability, as well as epigenetic silencing. Given the apparently opposing effects of Sp1, a more complete understanding of the function of Sp1 in cancer is required to validate its potential as a therapeutic target.
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                Author and article information

                Contributors
                Monika Jasek: +48 71 3709976 , jasek@iitd.pan.wroc.pl
                Journal
                Journal ID (nlm-ta): Tumour Biol
                Journal ID (iso-abbrev): Tumour Biol
                Title: Tumour Biology
                Publisher: Springer Netherlands (Dordrecht )
                ISSN (Print): 1010-4283
                ISSN (Electronic): 1423-0380
                Publication date (Electronic): 29 July 2016
                Publication date PMC-release: 29 July 2016
                Publication date Collection: October 2016
                Volume: 37
                Issue: 10
                Pages: 13617-13626
                Affiliations
                [1 ]Laboratory of Immunogenetics and Tissue Immunology, Department of Clinical Immunology, Ludwik Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, ul. Weigla 12, 53-114 Wroclaw, Poland
                [2 ]Chair and Department of Clinical Immunology, Medical University of Lublin, Chodzki 4a, 20-093 Lublin, Poland
                [3 ]Department of Genomics, Faculty of Biotechnology, University of Wrocław, ul. Fryderyka Joliot-Curie 14a, 50-383 Wroclaw, Poland
                [4 ]Department of Hematology, Neoplastic Diseases, and Bone Marrow Transplantation, Wroclaw Medical University, ul. Pasteura 1, 50-367 Wroclaw, Poland
                [5 ]Department of Experimental Therapy, Institute of Immunology and Experimental Therapy, Polish Academy of Science, ul. Weigla 12, 53-114 Wroclaw, Poland
                Article
                Publisher ID: 5182
                DOI: 10.1007/s13277-016-5182-z
                PMC ID: 5097080
                PubMed ID: 27468724
                SO-VID: 747b7a82-1eee-4625-8164-e56d016d7433
                Copyright © © The Author(s) 2016
                License:

                Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

                History
                Date received : 18 March 2016
                Date accepted : 12 July 2016
                Funding
                Funded by: National Science Centre Poland
                Award ID: N N402 680940.
                Award ID: N N402 682040
                Award Recipient :
                Funded by: State Committee for Scientific Research (Poland)
                Award ID: No. 2 PO5B 116 27
                Award Recipient :
                Categories
                Subject: Original Article
                Custom metadata
                issue-copyright-statement © International Society of Oncology and BioMarkers (ISOBM) 2016

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: cll,baff,baff-r,polymorphism
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: cll, baff, baff-r, polymorphism

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