Genome-wide association study of classical Hodgkin lymphoma identifies key regulators of disease susceptibility
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Karl-Heinz Jöckel | Julian Peto | K. D. Sørensen | Rosalind Eeles | Douglas Easton | Nick Orr | Asta Försti | Andreas Engert | Oleg Lenive | Per Hoffmann | Ali Amin Al Olama | Nora Pashayan | Federico Canzian | Hauke Thomsen | Kari Hemminki | Eleanor Kane | Eve Roman | Kenneth Muir | M. Nöthen | M. Kogevinas | S. Chanock | A. Wolk | R. Eeles | Z. Kote-Jarai | G. Giles | K. Muir | B. Henderson | J. Schleutker | J. Stanford | S. Ingles | E. John | C. Maier | R. Kaneva | J. Batra | D. Easton | C. Tangen | A. Kibel | P. Pharoah | J. Peto | D. Conti | N. Orr | P. Broderick | R. Houlston | D. Albanes | S. Weinstein | F. Schumacher | G. Cancel-Tassin | F. Wiklund | K. Hemminki | K. Jöckel | A. Dunning | B. Nordestgaard | H. Gronberg | M. Roobol | F. Menegaux | A. Swerdlow | S. Neuhausen | A. Försti | F. Canzian | F. Claessens | P. Law | V. Stevens | P. Hoffmann | K. Penney | T. Lightfoot | P. Townsend | D. Lessel | N. Usmani | B. Rosenstein | L. Mucci | H. Thomsen | Jeri Kim | L. Newcomb | Stella Koutros | S. Benlloch | R. Travis | N. Pashayan | C. Cybulski | M. Teixeira | M. Gago-Domínguez | L. Maehle | K. De Ruyck | C. West | A. Holroyd | O. Lenive | A. Sud | Giulia Orlando | R. Cooke | A. Engert | E. Roman | R. Jarrett | A. Lake | D. Montgomery | Paul Pharoah | Tracy Lightfoot | ZSofia Kote-Jarai | Alison Dunning | Peter Broderick | Anthony J. Swerdlow | Giulia Orlando | Amy Holroyd | Richard S. Houlston | Amit Sud | Philip J. Law | Miguel Inacio da Silva Filho | Lauren Wright | Rosie Cooke | Markus M. Nöthen | Elke Pogge von Strandmann | Annette Lake | Dorothy Montgomery | Ruth F. Jarrett | E. Kane | H. Brenner | Ana Vega | Lauren B Wright | A. Razack | M. I. S. Filho | E. P. Strandmann | D. E. Neal | Judith A. Clements | Jong Y. Park | Brian E. Christopher A. Sara Fredrick R. Ali Amin Al Son Henderson Haiman Benlloch Schumacher Olama | Sonja I. Berndt | C. Haiman | Yong-jie Lu | G. Cancel‐Tassin | R. Hamilton | D. Neal | A. Olama | Annette Lake | B. Henderson | M. Teixeira | Lisa F. Newcomb | Rosie Cooke | Dorothy Montgomery
[1] K. D. Sørensen,et al. Author Correction: Genome-wide association study of classical Hodgkin lymphoma identifies key regulators of disease susceptibility , 2019, Nature Communications.
[2] M. Nöthen,et al. A genome-wide association study identifies risk loci for childhood acute lymphoblastic leukemia at 10q26.13 and 12q23.1 , 2016, Leukemia.
[3] Alexis Battle,et al. Genetic variation in MHC proteins is associated with T cell receptor expression biases , 2016, Nature Genetics.
[4] P. Visscher,et al. Integration of summary data from GWAS and eQTL studies predicts complex trait gene targets , 2016, Nature Genetics.
[5] Daniel S. Himmelstein,et al. Meta-analysis of genome-wide association studies reveals genetic overlap between Hodgkin lymphoma and multiple sclerosis , 2016, International journal of epidemiology.
[6] J. Olsen,et al. Familial risk of non-Hodgkin lymphoma by sex, relationship, age at diagnosis and histology: a joint study from five Nordic countries , 2016, Leukemia.
[7] Manolis Kellis,et al. HaploReg v4: systematic mining of putative causal variants, cell types, regulators and target genes for human complex traits and disease , 2015, Nucleic Acids Res..
[8] Jonathan M. Cairns,et al. CHiCAGO: robust detection of DNA looping interactions in Capture Hi-C data , 2015, Genome Biology.
[9] Philip A. Ewels,et al. HiCUP: pipeline for mapping and processing Hi-C data , 2015, F1000Research.
[10] J. Olsen,et al. Risk of familial classical Hodgkin lymphoma by relationship, histology, age, and sex: a joint study from five Nordic countries. , 2015, Blood.
[11] J. Fellay,et al. Amino Acid Variation in HLA Class II Proteins Is a Major Determinant of Humoral Response to Common Viruses , 2015, American journal of human genetics.
[12] J. Rioux,et al. Genetic association analyses implicate aberrant regulation of innate and adaptive immunity genes in the pathogenesis of systemic lupus erythematosus , 2015, Nature Genetics.
[13] Casey S. Greene,et al. International genome-wide meta-analysis identifies new primary biliary cirrhosis risk loci and targetable pathogenic pathways , 2015, Nature Communications.
[14] Tom R. Gaunt,et al. Improved imputation of low-frequency and rare variants using the UK10K haplotype reference panel , 2015, Nature Communications.
[15] James T. Elder,et al. Widespread non-additive and interaction effects within HLA loci modulate the risk of autoimmune diseases , 2015, Nature Genetics.
[16] Philip A. Ewels,et al. Mapping long-range promoter contacts in human cells with high-resolution capture Hi-C , 2015, Nature Genetics.
[17] Christian Gieger,et al. Association of CLEC16A with human common variable immunodeficiency disorder and role in murine B cells , 2015, Nature Communications.
[18] Alexandra G. Smith,et al. Lymphoma incidence, survival and prevalence 2004–2014: sub-type analyses from the UK's Haematological Malignancy Research Network , 2015, British Journal of Cancer.
[19] K. Hemminki,et al. Heritability estimates on Hodgkin’s lymphoma: a genomic- versus population-based approach , 2014, European Journal of Human Genetics.
[20] M. Daly,et al. LD Score regression distinguishes confounding from polygenicity in genome-wide association studies , 2014, Nature Genetics.
[21] Gabriele Migliorini,et al. visPIG - A Web Tool for Producing Multi-Region, Multi-Track, Multi-Scale Plots of Genetic Data , 2014, PloS one.
[22] K. Basso,et al. microRNA 28 controls cell proliferation and is down-regulated in B-cell lymphomas , 2014, Proceedings of the National Academy of Sciences.
[23] C. Vinuesa,et al. Control of TFH cell numbers: why and how? , 2014, Immunology and cell biology.
[24] Jun S. Liu,et al. Genetics of rheumatoid arthritis contributes to biology and drug discovery , 2013 .
[25] P Boffetta,et al. A Meta-Analysis of Hodgkin Lymphoma Reveals 19p13.3 TCF3 as a Novel Susceptibility Locus , 2013, Nature Communications.
[26] Karl-Heinz Jöckel,et al. Variation at 3p24.1 and 6q23.3 influences the risk of Hodgkin’s Lymphoma , 2013, Nature Communications.
[27] M. Calaminici,et al. Defining characteristics of classical Hodgkin lymphoma microenvironment T-helper cells. , 2013, Blood.
[28] Buhm Han,et al. Imputing Amino Acid Polymorphisms in Human Leukocyte Antigens , 2013, PloS one.
[29] S. Jacobsen,et al. Transcriptional Repression of Gata3 Is Essential for Early B Cell Commitment , 2013, Immunity.
[30] Ellen T. Gelfand,et al. The Genotype-Tissue Expression (GTEx) project , 2013, Nature Genetics.
[31] W. Klapper,et al. Analyzing primary Hodgkin and Reed-Sternberg cells to capture the molecular and cellular pathogenesis of classical Hodgkin lymphoma. , 2012, Blood.
[32] R. Gascoyne,et al. Gene expression profiling of microdissected Hodgkin Reed-Sternberg cells correlates with treatment outcome in classical Hodgkin lymphoma. , 2012, Blood.
[33] Simon C. Potter,et al. Mapping cis- and trans-regulatory effects across multiple tissues in twins , 2012, Nature Genetics.
[34] Swneke D. Bailey,et al. Breast cancer risk-associated SNPs modulate the affinity of chromatin for FOXA1 and alter gene expression , 2012, Nature Genetics.
[35] Kristian Thorlund,et al. Evolution of Heterogeneity (I2) Estimates and Their 95% Confidence Intervals in Large Meta-Analyses , 2012, PloS one.
[36] H. Hjalgrim. On the aetiology of Hodgkin lymphoma. , 2012, Danish medical journal.
[37] Y. Kamatani,et al. Genome-wide association study of classical Hodgkin lymphoma and Epstein-Barr virus status-defined subgroups. , 2012, Journal of the National Cancer Institute.
[38] Avner Schlessinger,et al. ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI , 2012 .
[39] Simon C. Potter,et al. Genetic risk and a primary role for cell-mediated immune mechanisms in multiple sclerosis , 2011, Nature.
[40] Gonçalo R. Abecasis,et al. The variant call format and VCFtools , 2011, Bioinform..
[41] Edward P. Morris,et al. Structural basis for the subunit assembly of the anaphase-promoting complex , 2011, Nature.
[42] Tariq Ahmad,et al. Meta-analysis identifies 29 additional ulcerative colitis risk loci, increasing the number of confirmed associations to 47 , 2011, Nature Genetics.
[43] P. Visscher,et al. GCTA: a tool for genome-wide complex trait analysis. , 2011, American journal of human genetics.
[44] R. Küppers,et al. Mechanisms of aberrant GATA3 expression in classical Hodgkin lymphoma and its consequences for the cytokine profile of Hodgkin and Reed/Sternberg cells. , 2010, Blood.
[45] A. Ashworth,et al. A genome-wide association study of Hodgkin Lymphoma identifies new susceptibility loci at 2p16.1 (REL), 8q24.21, and 10p14 (GATA3) , 2010, Nature Genetics.
[46] D. Altshuler,et al. A map of human genome variation from population-scale sequencing , 2010, Nature.
[47] A. Morris,et al. Data quality control in genetic case-control association studies , 2010, Nature Protocols.
[48] W. Chan,et al. BCL6 promoter interacts with far upstream sequences with greatly enhanced activating histone modifications in germinal center B cells , 2010, Proceedings of the National Academy of Sciences.
[49] Trey Ideker,et al. A global network of transcription factors, involving E2A, EBF1 and Foxo1, that orchestrates the B cell fate , 2010, Nature Immunology.
[50] E. Taparowsky,et al. Batf coordinates multiple aspects of B and T cell function required for normal antibody responses , 2010, The Journal of experimental medicine.
[51] Tariq Ahmad,et al. Meta-analysis and imputation refines the association of 15q25 with smoking quantity , 2010, Nature Genetics.
[52] P. Deloukas,et al. Multiple common variants for celiac disease influencing immune gene expression , 2010, Nature Genetics.
[53] Michael R. Green,et al. Selective interaction between Trf3 and Taf3 required for early development and hematopoiesis , 2009, Developmental dynamics : an official publication of the American Association of Anatomists.
[54] M. Björkholm,et al. Autoimmunity and risk for Hodgkin’s lymphoma by subtype , 2009, Haematologica.
[55] R. Siebert,et al. Mutations of NFKBIA, encoding IκBα, are a recurrent finding in classical Hodgkin lymphoma but are not a unifying feature of non‐EBV‐associated cases , 2009, International journal of cancer.
[56] J. Romero,et al. Differential Genetic and Functional Markers of Second Neoplasias in Hodgkin's Disease Patients , 2009, Clinical Cancer Research.
[57] J. Gécz,et al. A UPF3-mediated regulatory switch that maintains RNA surveillance , 2009, Nature Structural &Molecular Biology.
[58] P. Donnelly,et al. A Flexible and Accurate Genotype Imputation Method for the Next Generation of Genome-Wide Association Studies , 2009, PLoS genetics.
[59] H. Qian,et al. Identification of tyrosine kinase, HCK, and tumor suppressor, BIN1, as potential mediators of AHI-1 oncogene in primary and transformed CTCL cells. , 2009, Blood.
[60] Hannah J. Whiteman,et al. Downregulation of RUNX1 by RUNX3 Requires the RUNX3 VWRPY Sequence and Is Essential for Epstein-Barr Virus-Driven B-Cell Proliferation , 2009, Journal of Virology.
[61] Ralf Küppers,et al. The biology of Hodgkin's lymphoma , 2009, Nature Reviews Cancer.
[62] H. Hjalgrim,et al. Infectious aetiology of Hodgkin and non‐Hodgkin lymphomas: a review of the epidemiological evidence , 2008, Journal of internal medicine.
[63] P. Sung,et al. BLAP18/RMI2, a novel OB-fold-containing protein, is an essential component of the Bloom helicase-double Holliday junction dissolvasome. , 2008, Genes & development.
[64] I. Arts. A review of the epidemiological evidence on tea, flavonoids, and lung cancer. , 2008, The Journal of nutrition.
[65] G. Reynolds,et al. Down-regulation of the TGF-beta target gene, PTPRK, by the Epstein-Barr virus encoded EBNA1 contributes to the growth and survival of Hodgkin lymphoma cells. , 2008, Blood.
[66] E. Vellenga,et al. HLA class II expression by Hodgkin Reed-Sternberg cells is an independent prognostic factor in classical Hodgkin's lymphoma. , 2007, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[67] P. Donnelly,et al. A new multipoint method for genome-wide association studies by imputation of genotypes , 2007, Nature Genetics.
[68] Simon C. Potter,et al. Genome-wide association study of 14,000 cases of seven common diseases and 3,000 shared controls , 2007, Nature.
[69] E. Roman,et al. Obesity and the risk of Hodgkin lymphoma (United Kingdom) , 2006, Cancer Causes & Control.
[70] G. Abecasis,et al. Joint analysis is more efficient than replication-based analysis for two-stage genome-wide association studies , 2006, Nature Genetics.
[71] P. Farrell,et al. RUNX expression and function in human B cells. , 2006, Critical reviews in eukaryotic gene expression.
[72] D. Clayton,et al. Population structure, differential bias and genomic control in a large-scale, case-control association study , 2005, Nature Genetics.
[73] C. Eaves,et al. Deregulated expression in Ph+ human leukemias of AHI-1, a gene activated by insertional mutagenesis in mouse models of leukemia. , 2004, Blood.
[74] G. M. Taylor,et al. The Scotland and Newcastle epidemiological study of Hodgkin’s disease: impact of histopathological review and EBV status on incidence estimates , 2003, Journal of clinical pathology.
[75] S. Hamilton-Dutoit,et al. Loss of B cell identity correlates with loss of B cell-specific transcription factors in Hodgkin/Reed-Sternberg cells of classical Hodgkin lymphoma , 2002, Oncogene.
[76] S. Thompson,et al. Quantifying heterogeneity in a meta‐analysis , 2002, Statistics in medicine.
[77] S. Alkan,et al. Characterization of NF-κB Expression in Hodgkin’s Disease: Inhibition of Constitutively Expressed NF-κB Results in Spontaneous Caspase-Independent Apoptosis in Hodgkin and Reed-Sternberg Cells , 2001, Modern Pathology.
[78] S. Alkan,et al. Characterization of NF-kappaB expression in Hodgkin's disease: inhibition of constitutively expressed NF-kappaB results in spontaneous caspase-independent apoptosis in Hodgkin and Reed-Sternberg cells. , 2001, Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc.
[79] G. M. Taylor,et al. Risk factors for Hodgkin's disease by Epstein-Barr virus (EBV) status: prior infection by EBV and other agents , 2000, British Journal of Cancer.
[80] L. Young,et al. Analysis of major histocompatibility complex class I, TAP expression, and LMP2 epitope sequence in Epstein-Barr virus-positive Hodgkin's disease. , 1998, Blood.
[81] G. Ghosh,et al. Crystal structure of p50/p65 heterodimer of transcription factor NF-κB bound to DNA , 1998, Nature.
[82] B. Dörken,et al. Constitutive nuclear factor-kappaB-RelA activation is required for proliferation and survival of Hodgkin's disease tumor cells. , 1997, The Journal of clinical investigation.
[83] B. Nathwani,et al. Concordance for Hodgkin's disease in identical twins suggesting genetic susceptibility to the young-adult form of the disease. , 1995, The New England journal of medicine.
[84] H. Erlich,et al. Two new HLA DRB1 alleles found in African Americans: implications for balancing selection at positions 57 and 86. , 1992, Tissue antigens.
[85] J. Rothbard,et al. Effect of natural polymorphism at residue 86 of the HLA-DR beta chain on peptide binding. , 1991, Journal of immunology.