For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
52
views
15
references
 Top references
cited by
43
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      771
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: not found

      Loci on 7p12.2, 10q21.2 and 14q11.2 are associated with risk of childhood acute lymphoblastic leukemia

      research-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          To identify risk variants for childhood acute lymphoblastic leukemia (ALL) we conducted a genome-wide association study of 2 case-control series, analyzing the genotypes of 291,423 tagging SNP genotypes in a total of 907 ALL cases and 2,398 controls. We identified risk loci for ALL at 7p12.2 ( IKZF1, rs4132601; OR = 1.69, P = 1.20 x 10 -19), 10q21.2 ( ARIDB5, rs7089424; OR = 1.65, P = 6.69 x 10 -19) and 14q11.2 ( CEBPE, rs2239633; OR = 1.34, P = 2.88 x 10 -7). The 10q21.2 ( ARIDB5) risk association appears to be selective for the subset of B-cell precursor ALL with hyperdiploidy. These data show that common low-penetrance susceptibility alleles contribute to the risk of developing childhood ALL and provide novel insight into disease causation of this hematological cancer; notably all 3 risk variants map to genes involved in transcriptional regulation and differentiation of B-cell progenitors.

          Related collections

          Most cited references15

          • Record: found
          • Abstract: not found
          • Article: not found

          Acute lymphoblastic leukemia.

          Ching-Hon Pui, Mary Relling, James R. Downing (2004)
          Article 0 comments Cited 236 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            A genome-wide association study identifies colorectal cancer susceptibility loci on chromosomes 10p14 and 8q23.3.

            Ian PM Tomlinson, Emily Webb, Luis Carvajal-Carmona … (2008)
            To identify colorectal cancer (CRC) susceptibility alleles, we conducted a genome-wide association study. In phase 1, we genotyped 550,163 tagSNPs in 940 familial colorectal tumor cases (627 CRC, 313 high-risk adenoma) and 965 controls. In phase 2, we genotyped 42,708 selected SNPs in 2,873 CRC cases and 2,871 controls. In phase 3, we evaluated 11 SNPs showing association at P < 10(-4) in a joint analysis of phases 1 and 2 in 4,287 CRC cases and 3,743 controls. Two SNPs were taken forward to phase 4 genotyping (10,731 CRC cases and 10,961 controls from eight centers). In addition to the previously reported 8q24, 15q13 and 18q21 CRC risk loci, we identified two previously unreported associations: rs10795668, located at 10p14 (P = 2.5 x 10(-13) overall; P = 6.9 x 10(-12) replication), and rs16892766, at 8q23.3 (P = 3.3 x 10(-18) overall; P = 9.6 x 10(-17) replication), which tags a plausible causative gene, EIF3H. These data provide further evidence for the 'common-disease common-variant' model of CRC predisposition.
            Article 0 comments Cited 176 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Infection, immune responses and the aetiology of childhood leukaemia.

              Mel F Greaves (2006)
              Childhood leukaemia is the principal subtype of paediatric cancer and, despite success in treatment, its causes remain enigmatic. A plethora of candidate environmental exposures have been proposed, but most lack a biological rationale or consistent epidemiological evidence. Although there might not be a single or exclusive cause, an abnormal immune response to common infection(s) has emerged as a plausible aetiological mechanism.
              Article 0 comments Cited 159 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Journal
                Journal ID (nlm-journal-id): 9216904
                Journal ID (pubmed-jr-id): 2419
                Journal ID (nlm-ta): Nat Genet
                Journal ID (iso-abbrev): Nat. Genet.
                Title: Nature genetics
                ISSN (Print): 1061-4036
                ISSN (Electronic): 1546-1718
                Publication date Nihms-submitted: 26 May 2016
                Publication date (Electronic): 16 August 2009
                Publication date (Print): September 2009
                Publication date PMC-release: 21 June 2016
                Volume: 41
                Issue: 9
                Pages: 1006-1010
                Affiliations
                [1 ]Section of Cancer Genetics, Institute of Cancer Research, Sutton, Surrey, SM2 5NG, UK
                [2 ]Yorkshire Regional Genetic Service, St James’s University Hospital, Beckett Street, Leeds, LS9 7T, UK
                [3 ]Department of Paediatric and Adolescent Oncology and Haematology, St James University Hospital, Leeds, LS9 7T, UK
                [4 ]Epidemiology and Genetics Unit, Department of Health Sciences, University of York, York Y010 5DD, UK
                [5 ]Northern Institute for Cancer Research, Newcastle University, Framlington Place, Newcastle upon Tyne, NE2 4HH, UK
                [6 ]Molecular and Population Genetics, Wellcome Trust Centre for Human Genetics, Oxford, OX3 7BN, UK
                [7 ]Cancer Immunogenetics Group, School of Cancer Sciences, University of Manchester, Research Floor, St Mary’s Hospital, Manchester, M13 0JH, UK
                [8 ]Section of Haemato-oncology, Institute of Cancer Research, Sutton, Surrey, SM2 5NG, UK
                Author notes
                [* ]Corresponding author: Richard.houlston@ 123456icr.ac.uk , Tel: +44 (0) 208 722 4175, Fax: +44 (0) 208 722 4365
                Article
                Manuscript ID: EMS27409
                DOI: 10.1038/ng.430
                PMC ID: 4915548
                PubMed ID: 19684604
                SO-VID: e8091179-8f28-4c6b-9627-1fb70b218887
                License:

                Users may view, print, copy, and download text and data-mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use: http://www.nature.com/authors/editorial_policies/license.html#terms

                History
                Categories
                Subject: Article

                ScienceOpen disciplines: Genetics
                Data availability:
                ScienceOpen disciplines: Genetics

                Comments

                Comment on this article

                scite_

                Similar content771

                See all similar

                Cited by127

                See all cited by

                Most referenced authors691

                See all reference authors