Genetic association with rheumatoid arthritis—Genetic Analysis Workshop 15: summary of contributions from Group 2

The papers in presentation group 2 of Genetic Analysis Workshop 15 (GAW15) conducted association analyses of rheumatoid arthritis data. The analyses were carried out primarily in the data provided by the North American Rheumatoid Arthritis Consortium (NARAC). One group conducted analyses in the data provided by the Canadian Rheumatoid Arthritis Genetics Study (CRAGS). Analysis strategies included genome‐wide scans, the examination of candidate genes, and investigations of a region of interest on chromosome 18q21. Most authors employed relatively new methods, proposed extensions of existing methods, or introduced completely novel methods for aspects of association analysis. There were several common observations; a group of papers using a variety of methods found stronger association, on chromosomes 6 and 18 and in candidate gene PTPN22 among women with early onset. Generally, models that considered haplotypes or multiple markers showed stronger evidence for association than did single marker analyses. Genet. Epidemiol. 31 (Suppl. 1):S12–S21, 2007. © 2007 Wiley‐Liss, Inc.

[1]  Sharon R Browning,et al.  Multilocus analysis of GAW15 NARAC chromosome 18 case-control data , 2007, BMC proceedings.

[2]  Xiuqing Guo,et al.  Evaluating gene × gene and gene × smoking interaction in rheumatoid arthritis using candidate genes in GAW15 , 2007, BMC Proceedings.

[3]  Annette Lee,et al.  Data for Genetic Analysis Workshop (GAW) 15 Problem 2, genetic causes of rheumatoid arthritis and associated traits , 2007, BMC proceedings.

[4]  A. Califano,et al.  Pattern-based mining strategy to detect multi-locus association and gene × environment interaction , 2007, BMC proceedings.

[5]  Cheng Hu,et al.  Impact of marker density on the accuracy of association mapping , 2007, BMC proceedings.

[6]  S. Tezenas du Montcel,et al.  Modeling of PTPN22 and HLA-DRB1 susceptibility to rheumatoid arthritis , 2007, BMC proceedings.

[7]  D. Schaid,et al.  Application of sequential haplotype scan methods to case-control data , 2007, BMC proceedings.

[8]  N. Morton,et al.  Mapping a gene for rheumatoid arthritis on chromosome 18q21 , 2007, BMC proceedings.

[9]  Iuliana Ionita-Laza,et al.  Constructing gene association networks for rheumatoid arthritis using the backward genotype-trait association (BGTA) algorithm , 2007, BMC proceedings.

[10]  M. Wilcox,et al.  Empirically derived subgroups in rheumatoid arthritis: association with single-nucleotide polymorphisms on chromosome 6 , 2007, BMC proceedings.

[11]  Cheng Hu,et al.  Association mapping of susceptibility loci for rheumatoid arthritis , 2007, BMC proceedings.

[12]  Kristina Allen-Brady,et al.  Meta-genetic association of rheumatoid arthritis and PTPN22 using PedGenie 2.1 , 2007, BMC proceedings.

[13]  Zhi Wei,et al.  Genome-wide linkage and association analysis of rheumatoid arthritis in a Canadian population , 2007, BMC proceedings.

[14]  Zhaoxia Yu,et al.  Sequential haplotype scan methods for association analysis , 2007, Genetic epidemiology.

[15]  Tian Zheng,et al.  Backward Genotype-Trait Association (BGTA)-Based Dissection of Complex Traits in Case-Control Designs , 2006, Human Heredity.

[16]  Sharon R Browning,et al.  Multilocus association mapping using variable-length Markov chains. , 2006, American journal of human genetics.

[17]  Nicola J. Camp,et al.  PedGenie: an analysis approach for genetic association testing in extended pedigrees and genealogies of arbitrary size , 2006, BMC Bioinformatics.

[18]  Paul Scheet,et al.  A fast and flexible statistical model for large-scale population genotype data: applications to inferring missing genotypes and haplotypic phase. , 2006, American journal of human genetics.

[19]  Elizabeth W Karlson,et al.  Replication of putative candidate-gene associations with rheumatoid arthritis in >4,000 samples from North America and Sweden: association of susceptibility with PTPN22, CTLA4, and PADI4. , 2005, American journal of human genetics.

[20]  Steven J. Schrodi,et al.  PTPN22 genetic variation: evidence for multiple variants associated with rheumatoid arthritis. , 2005, American journal of human genetics.

[21]  M. Daly,et al.  Haploview: analysis and visualization of LD and haplotype maps , 2005, Bioinform..

[22]  Tian Zheng,et al.  Backward Haplotype Transmission Association (BHTA) Algorithm – A Fast Multiple-Marker Screening Method , 2002, Human Heredity.

[23]  J. H. Moore,et al.  Multifactor-dimensionality reduction reveals high-order interactions among estrogen-metabolism genes in sporadic breast cancer. , 2001, American journal of human genetics.

[24]  P. Donnelly,et al.  A new statistical method for haplotype reconstruction from population data. , 2001, American journal of human genetics.

[25]  G. Lathrop,et al.  A new method to test genetic models in HLA associated diseases: the MASC method , 1988, Annals of human genetics.

[26]  K Y Liang,et al.  Longitudinal data analysis for discrete and continuous outcomes. , 1986, Biometrics.

[27]  J. Edwards.  The genetic basis of common disease , 1963 .

[28]  N. Morton,et al.  Genome scanning by composite likelihood. , 2007, American journal of human genetics.

[29]  C. Carlson,et al.  Selecting a maximally informative set of single-nucleotide polymorphisms for association analyses using linkage disequilibrium. , 2004, American journal of human genetics.

[30]  G. Abecasis,et al.  Merlin—rapid analysis of dense genetic maps using sparse gene flow trees , 2002, Nature Genetics.

[31]  Richard A. King,et al.  The genetic basis of common diseases. , 2002 .