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Identification of multiple rare variants associated with a disease
Identifying rare variants that are responsible for complex disease has been promoted by advances in sequencing technologies. However, statistical methods that can handle the vast amount of data generated and that can interpret the complicated relationship between disease and these variants have lagg...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2011
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3287826/ https://www.ncbi.nlm.nih.gov/pubmed/22373445 http://dx.doi.org/10.1186/1753-6561-5-S9-S103 |
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author | Jung, Jeesun Dantzer, Jessica Liu, Yunlong |
author_facet | Jung, Jeesun Dantzer, Jessica Liu, Yunlong |
author_sort | Jung, Jeesun |
collection | PubMed |
description | Identifying rare variants that are responsible for complex disease has been promoted by advances in sequencing technologies. However, statistical methods that can handle the vast amount of data generated and that can interpret the complicated relationship between disease and these variants have lagged. We apply a zero-inflated Poisson regression model to take into account the excess of zeros caused by the extremely low frequency of the 24,487 exonic variants in the Genetic Analysis Workshop 17 data. We grouped the 697 subjects in the data set as Europeans, Asians, and Africans based on principal components analysis and found the total number of rare variants per gene for each individual. We then analyzed these collapsed variants based on the assumption that rare variants are enriched in a group of people affected by a disease compared to a group of unaffected people. We also tested the hypothesis with quantitative traits Q1, Q2, and Q4. Analyses performed on the combined 697 individuals and on each ethnic group yielded different results. For the combined population analysis, we found that UGT1A1, which was not part of the simulation model, was associated with disease liability and that FLT1, which was a causal locus in the simulation model, was associated with Q1. Of the causal loci in the simulation models, FLT1 and KDR were associated with Q1 and VNN1 was correlated with Q2. No significant genes were associated with Q4. These results show the feasibility and capability of our new statistical model to detect multiple rare variants influencing disease risk. |
format | Online Article Text |
id | pubmed-3287826 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2011 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-32878262012-02-28 Identification of multiple rare variants associated with a disease Jung, Jeesun Dantzer, Jessica Liu, Yunlong BMC Proc Proceedings Identifying rare variants that are responsible for complex disease has been promoted by advances in sequencing technologies. However, statistical methods that can handle the vast amount of data generated and that can interpret the complicated relationship between disease and these variants have lagged. We apply a zero-inflated Poisson regression model to take into account the excess of zeros caused by the extremely low frequency of the 24,487 exonic variants in the Genetic Analysis Workshop 17 data. We grouped the 697 subjects in the data set as Europeans, Asians, and Africans based on principal components analysis and found the total number of rare variants per gene for each individual. We then analyzed these collapsed variants based on the assumption that rare variants are enriched in a group of people affected by a disease compared to a group of unaffected people. We also tested the hypothesis with quantitative traits Q1, Q2, and Q4. Analyses performed on the combined 697 individuals and on each ethnic group yielded different results. For the combined population analysis, we found that UGT1A1, which was not part of the simulation model, was associated with disease liability and that FLT1, which was a causal locus in the simulation model, was associated with Q1. Of the causal loci in the simulation models, FLT1 and KDR were associated with Q1 and VNN1 was correlated with Q2. No significant genes were associated with Q4. These results show the feasibility and capability of our new statistical model to detect multiple rare variants influencing disease risk. BioMed Central 2011-11-29 /pmc/articles/PMC3287826/ /pubmed/22373445 http://dx.doi.org/10.1186/1753-6561-5-S9-S103 Text en Copyright ©2011 Jung et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Proceedings Jung, Jeesun Dantzer, Jessica Liu, Yunlong Identification of multiple rare variants associated with a disease |
title | Identification of multiple rare variants associated with a disease |
title_full | Identification of multiple rare variants associated with a disease |
title_fullStr | Identification of multiple rare variants associated with a disease |
title_full_unstemmed | Identification of multiple rare variants associated with a disease |
title_short | Identification of multiple rare variants associated with a disease |
title_sort | identification of multiple rare variants associated with a disease |
topic | Proceedings |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3287826/ https://www.ncbi.nlm.nih.gov/pubmed/22373445 http://dx.doi.org/10.1186/1753-6561-5-S9-S103 |
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