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Volume 3 Supplement 7

Genetic Analysis Workshop 16

Proceedings

Genetic Analysis Workshop 16. Go to conference site.

St Louis, MO, USA17-20 September 2008

Page 1 of 3

  1. Rheumatoid arthritis (RA) is a complex, chronic inflammatory disease implicated to have several plausible candidate loci; however, these may not account for all the genetic variations underlying RA. Common dis...

    Authors: Odity Mukherjee, Krishna Rao Sanapala, Padmanabhan Anbazhagana and Saurabh Ghosh
    Citation: BMC Proceedings 2009 3(Suppl 7):S82
  2. For Genetic Analysis Workshop 16 Problem 1, we provided data for genome-wide association analysis of rheumatoid arthritis. Single-nucleotide polymorphism (SNP) genotype data were provided for 868 cases and 119...

    Authors: Christopher I Amos, Wei Vivien Chen, Michael F Seldin, Elaine F Remmers, Kimberly E Taylor, Lindsey A Criswell, Annette T Lee, Robert M Plenge, Daniel L Kastner and Peter K Gregersen
    Citation: BMC Proceedings 2009 3(Suppl 7):S2
  3. Genetic Analysis Workshop 16 (GAW16) Problem 2 presented data from the Framingham Heart Study (FHS), an observational, prospective study of risk factors for cardiovascular disease begun in 1948. Data have been...

    Authors: L Adrienne Cupples, Nancy Heard-Costa, Monica Lee and Larry D Atwood
    Citation: BMC Proceedings 2009 3(Suppl 7):S3
  4. The Genetic Analysis Workshop (GAW) 16 Problem 3 comprises simulated phenotypes emulating the lipid domain and its contribution to cardiovascular disease risk. For each replication there were 6,476 subjects in...

    Authors: Aldi T Kraja, Robert Culverhouse, E Warwick Daw, Jun Wu, Andrew Van Brunt, Michael A Province and Ingrid B Borecki
    Citation: BMC Proceedings 2009 3(Suppl 7):S4
  5. Several methods have been proposed to impute genotypes at untyped markers using observed genotypes and genetic data from a reference panel. We used the Genetic Analysis Workshop 16 rheumatoid arthritis case-co...

    Authors: Joanna M Biernacka, Rui Tang, Jia Li, Shannon K McDonnell, Kari G Rabe, Jason P Sinnwell, David N Rider, Mariza de Andrade, Ellen L Goode and Brooke L Fridley
    Citation: BMC Proceedings 2009 3(Suppl 7):S5
  6. Due to the growing need to combine data across multiple studies and to impute untyped markers based on a reference sample, several analytical tools for imputation and analysis of missing genotypes have been de...

    Authors: Brooke L Fridley, Shannon K McDonnell, Kari G Rabe, Rui Tang, Joanna M Biernacka, Jason P Sinnwell, David N Rider and Ellen L Goode
    Citation: BMC Proceedings 2009 3(Suppl 7):S7
  7. To analyze multiple single-nucleotide polymorphisms simultaneously when the number of markers is much larger than the number of studied individuals, as is the situation we have in genome-wide association studi...

    Authors: Soonil Kwon, Jinrui Cui, Shannon L Rhodes, Donald Tsiang, Jerome I Rotter and Xiuqing Guo
    Citation: BMC Proceedings 2009 3(Suppl 7):S9
  8. The results from association studies are usually summarized by a measure of evidence of association (frequentist or Bayesian probability values) that does not directly reflect the impact of the detected signal...

    Authors: Justo Lorenzo Bermejo, Christine Fischer, Anke Schulz, Nadine Cremer, Rebecca Hein, Lars Beckmann, Jenny Chang-Claude and Kari Hemminki
    Citation: BMC Proceedings 2009 3(Suppl 7):S10
  9. The availability of very large number of markers by modern technology makes genome-wide association studies very popular. The usual approach is to test single-nucleotide polymorphisms (SNPs) one at a time for ...

    Authors: George Mathew, Hongyan Xu and Varghese George
    Citation: BMC Proceedings 2009 3(Suppl 7):S11
  10. There is a long-established association between rheumatoid arthritis and HLA-DRβ1. The shared epitope (SE) allele is an indicator of the presence of any of the HLA-DRβ1 alleles associated with RA. Other autoan...

    Authors: Abigail G Matthews, Jia Li, Chunsheng He, Jurg Ott and Mariza de Andrade
    Citation: BMC Proceedings 2009 3(Suppl 7):S12
  11. The North American Rheumatoid Arthritis Consortium case-control study collected case participants across the United States and control participants from New York. More than 500,000 single-nucleotide polymorphi...

    Authors: Sara M Sarasua, Julianne S Collins, Dhelia M Williamson, Glen A Satten and Andrew S Allen
    Citation: BMC Proceedings 2009 3(Suppl 7):S13
  12. We conducted a search for non-chromosome 6 genes that may increase risk for rheumatoid arthritis (RA). Our approach was to retrospectively ascertain three "extreme" subsamples from the North American Rheumatoi...

    Authors: Brian K Suarez, Robert Culverhouse, Carol H Jin and Anthony L Hinrichs
    Citation: BMC Proceedings 2009 3(Suppl 7):S15
  13. Currently, genome-wide association studies (GWAS) are conducted by collecting a massive number of SNPs (i.e., large p) for a relatively small number of individuals (i.e., small n) and associations are made betwee...

    Authors: Min Zhang, Yanzhu Lin, Libo Wang, Vitara Pungpapong, James C Fleet and Dabao Zhang
    Citation: BMC Proceedings 2009 3(Suppl 7):S17
  14. Genetic association of population-based quantitative trait data has traditionally been analyzed using analysis of variance (ANOVA). However, violations of certain statistical assumptions may lead to false-posi...

    Authors: Saurabh Ghosh, Krishna Rao Sanapala, Abhik Ghosh and Sujatro Chakladar
    Citation: BMC Proceedings 2009 3(Suppl 7):S18
  15. Many phenotypes may be influenced by the prenatal environment of the mother and/or maternal care, and these maternal effects may have a heritable component. We have implemented in the computer program SOLAR a ...

    Authors: Jack W Kent Jr, Charles P Peterson, Thomas D Dyer, Laura Almasy and John Blangero
    Citation: BMC Proceedings 2009 3(Suppl 7):S19
  16. Genome-wide associations between single-nucleotide polymorphisms and clinical traits were simultaneously conducted using penalized orthogonal-components regression. This method was developed to identify the ge...

    Authors: Yanzhu Lin, Min Zhang, Libo Wang, Vitara Pungpapong, James C Fleet and Dabao Zhang
    Citation: BMC Proceedings 2009 3(Suppl 7):S20
  17. Because multiple loci control complex diseases, there is great interest in testing markers simultaneously instead of one by one. In this paper, we applied two model selection algorithms: the stochastic search ...

    Authors: Sudeep Srivastava and Liang Chen
    Citation: BMC Proceedings 2009 3(Suppl 7):S21
  18. Population stratification is one of the major causes of spurious associations in association studies. A unified association approach based on principal-component analysis can overcome the effect of population ...

    Authors: Xiangqing Sun, Tao Feng, Yeunjoo Song, Robert C Elston and Xiaofeng Zhu
    Citation: BMC Proceedings 2009 3(Suppl 7):S22
  19. Most genetic association studies only genotype a small proportion of cataloged single-nucleotide polymorphisms (SNPs) in regions of interest. With the catalogs of high-density SNP data available (e.g., HapMap)...

    Authors: Douglas K Childers, Guolian Kang, Nianjun Liu, Guimin Gao and Kui Zhang
    Citation: BMC Proceedings 2009 3(Suppl 7):S24
  20. The current trend in genome-wide association studies is to identify regions where the true disease-causing genes may lie by evaluating thousands of single-nucleotide polymorphisms (SNPs) across the whole genom...

    Authors: Seoae Cho, Haseong Kim, Sohee Oh, Kyunga Kim and Taesung Park
    Citation: BMC Proceedings 2009 3(Suppl 7):S25
  21. We compared family-based single-marker association analysis using Merlin and multi-marker analysis using LASSO (least absolute shrinkage and selection operator) for the low-density lipoprotein phenotype at the...

    Authors: Yun Ju Sung, Treva K Rice, Gang Shi, C Charles Gu and DC Rao
    Citation: BMC Proceedings 2009 3(Suppl 7):S27
  22. The interaction among multiple genes and environmental factors can affect an individual's susceptibility to disease. Some genes may not show strong marginal associations when they affect disease risk through i...

    Authors: Zheyang Wu, Chatchawit Aporntewan, David H Ballard, Ji Young Lee, Joon Sang Lee and Hongyu Zhao
    Citation: BMC Proceedings 2009 3(Suppl 7):S29
  23. Many autoimmune diseases share similar underlying pathology and have a tendency to cluster within families, giving rise to the concept of shared susceptibility genes among them. In the Genetic Analysis Worksho...

    Authors: Harshal Deshmukh, Xana Kim-Howard and Swapan K Nath
    Citation: BMC Proceedings 2009 3(Suppl 7):S31
  24. The Genetic Analysis Workshop 16 rheumatoid arthritis data include a set of 868 cases and 1194 controls genotyped at 545,080 single-nucleotide polymorphisms (SNPs) from the Illumina 550 k chip. We focus on inv...

    Authors: Wei Guo, Chin-yuan Liang and Shili Lin
    Citation: BMC Proceedings 2009 3(Suppl 7):S32
  25. Using single-nucleotide polymorphisms (SNPs), we sought to predict classical class I and class II human leukocyte antigen (HLA) alleles, and test for their associations with rheumatoid arthritis (RA) in the No...

    Authors: Mathieu Lemire
    Citation: BMC Proceedings 2009 3(Suppl 7):S33
  26. Recent genome-wide association studies on several complex diseases have focused on individual single-nucleotide polymorphism (SNP) analysis; however, not many studies have reported interactions among genes per...

    Authors: Jungsun Park, Junghyun Namkung, Mina Jhun and Taesung Park
    Citation: BMC Proceedings 2009 3(Suppl 7):S34
  27. The high genomic density of the single-nucleotide polymorphism (SNP) sets that are typically surveyed in genome-wide association studies (GWAS) now allows the application of haplotype-based methods. Although t...

    Authors: Heejung Shim, Hyonho Chun, Corinne D Engelman and Bret A Payseur
    Citation: BMC Proceedings 2009 3(Suppl 7):S35
  28. Genome-wide association studies often involve testing hundreds of thousands of single-nucleotide polymorphisms (SNPs). These tests may be highly correlated because of linkage disequilibrium among SNPs. Multipl...

    Authors: Guolian Kang, Douglas K Childers, Nianjun Liu, Kui Zhang and Guimin Gao
    Citation: BMC Proceedings 2009 3(Suppl 7):S38
  29. In high-dimensional studies such as genome-wide association studies, the correction for multiple testing in order to control total type I error results in decreased power to detect modest effects. We present a...

    Authors: Elena Parkhomenko, David Tritchler, Mathieu Lemire, Pingzhao Hu and Joseph Beyene
    Citation: BMC Proceedings 2009 3(Suppl 7):S40
  30. Metabolic syndrome, by definition, is the manifestation of multiple, correlated metabolic impairments. It is known to have both strong environmental and genetic contributions. However, isolating genetic varian...

    Authors: Allison R Baker, Robert J Goodloe, Emma K Larkin, Dan J Baechle, Yeunjoo E Song, Lynette S Phillips and Courtney L Gray-McGuire
    Citation: BMC Proceedings 2009 3(Suppl 7):S42
  31. Rheumatoid arthritis is inherited in a complex manner. So far several single susceptibility genes, such as PTPN22, STAT4, and TRAF1-C5, have been identified. However, it is presumed that some genes may interact t...

    Authors: Xiaoqi Cui, Qiuying Sha, Shuanglin Zhang and Huann-Sheng Chen
    Citation: BMC Proceedings 2009 3(Suppl 7):S43
  32. We propose the use of latent growth curve model to assess the influence of genetic, environmental, demographic, and lifestyle factors on multiple phenotypes related to coronary heart disease. We model four qua...

    Authors: Jemila S Hamid, Nicole M Roslin, Andrew D Paterson and Joseph Beyene
    Citation: BMC Proceedings 2009 3(Suppl 7):S44
  33. The phrase "mendelian randomization" has become associated with the use of genetic polymorphisms to uncover causal relationships between phenotypic variables. The statistical methods useful in mendelian random...

    Authors: Nathan J Morris, Courtney Gray-McGuire and Catherine M Stein
    Citation: BMC Proceedings 2009 3(Suppl 7):S45
  34. Multiple single-nucleotide polymorphisms have been associated with low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and triglyceride (TG) levels. In this paper, we eva...

    Authors: Stephen R Piccolo, Ryan P Abo, Kristina Allen-Brady, Nicola J Camp, Stacey Knight, Jeffrey L Anderson and Benjamin D Horne
    Citation: BMC Proceedings 2009 3(Suppl 7):S46
  35. Cardiovascular diseases are associated with combinations of phenotypic traits, which are in turn caused by a combination of environmental and genetic factors. Because of the diversity of pathways that may lead...

    Authors: Sandra Waaijenborg and Aeilko H Zwinderman
    Citation: BMC Proceedings 2009 3(Suppl 7):S47
  36. Genetic epidemiology studies often adjust for numerous potential confounders, yet the influences of confounder misclassification and selection bias are rarely considered. We used simulated data to evaluate the...

    Authors: Christy L Avery, Keri L Monda and Kari E North
    Citation: BMC Proceedings 2009 3(Suppl 7):S48

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