22 results on '"Williams, Scott M."'
Search Results
2. Expanding human variation at PLOS Genetics
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Barsh, Gregory S., primary, Copenhaver, Gregory P., additional, Tang, Hua, additional, and Williams, Scott M., additional
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- 2022
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3. Global variation in sequencing impedes SARS-CoV-2 surveillance
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Crawford, Dana C., primary and Williams, Scott M., additional
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- 2021
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4. Interaction between host genes and Mycobacterium tuberculosis lineage can affect tuberculosis severity: Evidence for coevolution?
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McHenry, Michael L., primary, Bartlett, Jacquelaine, additional, Igo, Robert P., additional, Wampande, Eddie M., additional, Benchek, Penelope, additional, Mayanja-Kizza, Harriet, additional, Fluegge, Kyle, additional, Hall, Noemi B., additional, Gagneux, Sebastien, additional, Tishkoff, Sarah A., additional, Wejse, Christian, additional, Sirugo, Giorgio, additional, Boom, W. Henry, additional, Joloba, Moses, additional, Williams, Scott M., additional, and Stein, Catherine M., additional
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- 2020
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5. Evaluating the strength of genetic results: Risks and responsibilities
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Barsh, Gregory S., primary, Cooper, Gregory M., additional, Copenhaver, Gregory P., additional, Sirugo, Giorgio, additional, Tang, Hua, additional, and Williams, Scott M., additional
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- 2019
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6. Whole exome sequencing reveals HSPA1L as a genetic risk factor for spontaneous preterm birth
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Huusko, Johanna M., Karjalainen, Minna K., Graham, Britney E., Zhang, Ge, Farrow, Emily G., Miller, Neil A., Jacobsson, Bo, Eidem, Haley R., Murray, Jeffrey C., Bedell, Bruce, Breheny, Patrick, Brown, Noah W., Bødker, Frans L., Litterman, Nadia K., Jiang, Pan-Pan, Russell, Laura, Hinds, David A., Hu, Youna, Rokas, Antonis, Teramo, Kari, Christensen, Kaare, Williams, Scott M., Rämet, Mika, Kingsmore, Stephen F., Ryckman, Kelli K., Hallman, Mikko, and Muglia, Louis J.
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Male ,Models, Molecular ,Maternal Health ,Biochemistry ,Heat Shock Response ,Recurrence ,Risk Factors ,Pregnancy ,Medicine and Health Sciences ,Macromolecular Structure Analysis ,Exome ,Post-Translational Modification ,Phosphorylation ,Finland ,Cellular Stress Responses ,Obstetrics and Gynecology ,Software Engineering ,Genomics ,Adenosine Diphosphate ,Cell Processes ,Premature Birth ,Engineering and Technology ,Female ,Signal Transduction ,Research Article ,Quality Control ,Protein Structure ,Computer and Information Sciences ,Preterm Birth ,Polymorphism, Single Nucleotide ,Cell Line ,Receptors, Glucocorticoid ,Exome Sequencing ,Industrial Engineering ,Genome-Wide Association Studies ,Genetics ,Humans ,Genetic Predisposition to Disease ,HSP70 Heat-Shock Proteins ,Molecular Biology ,Software Tools ,Infant, Newborn ,Biology and Life Sciences ,Computational Biology ,Proteins ,Human Genetics ,Estrogens ,Cell Biology ,Fibroblasts ,Genome Analysis ,Hormones ,Pregnancy Complications ,Case-Control Studies ,Birth ,Women's Health ,Genome-Wide Association Study - Abstract
Preterm birth is a leading cause of morbidity and mortality in infants. Genetic and environmental factors play a role in the susceptibility to preterm birth, but despite many investigations, the genetic basis for preterm birth remain largely unknown. Our objective was to identify rare, possibly damaging, nucleotide variants in mothers from families with recurrent spontaneous preterm births (SPTB). DNA samples from 17 Finnish mothers who delivered at least one infant preterm were subjected to whole exome sequencing. All mothers were of northern Finnish origin and were from seven multiplex families. Additional replication samples of European origin consisted of 93 Danish sister pairs (and two sister triads), all with a history of a preterm delivery. Rare exonic variants (frequency, Author summary Preterm birth is the leading cause of infant mortality, and prematurity is further associated with serious morbidities in later life. Genetic and environmental risk factors play a role in the susceptibility to preterm birth. Despite numerous studies, the genetic basis for preterm birth remains poorly defined. We investigated the presence of rare, possibly risk associated nucleotide variants in mothers with spontaneous preterm births (SPTB). The first set of mothers with family history of recurrent preterm births was of northern Finnish origin. An additional set of mothers (sister pairs, both giving birth preterm) of European origin was also studied. Whole exome sequencing identified multiple rare, likely damaging HSPA1L variants in several families affected by SPTB, and this gene was associated with the glucocorticoid receptor signaling pathway. Potential involvement of one of the HSPA1L variants in SPTB was further supported by large GWAS dataset. In addition, this variant alters protein post-translational modification potential, and thus may affect protein stability and its function as a chaperone.
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- 2018
7. The Plight of Muntaser Ibrahim
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Sirugo, Giorgio, primary, Williams, Scott M., additional, Tishkoff, Sarah A., additional, Cordell, Heather J., additional, Marchini, Jonathan, additional, Barsh, Gregory S., additional, and Copenhaver, Gregory P., additional
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- 2019
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8. Doubling down on forensic twin studies
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Copenhaver, Gregory P., primary, Weir, Bruce, additional, Rothstein, Mark, additional, Tang, Hua, additional, Williams, Scott M., additional, and Barsh, Gregory S., additional
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- 2018
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9. Widespread epistasis regulates glucose homeostasis and gene expression
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Chen, Anlu, primary, Liu, Yang, additional, Williams, Scott M., additional, Morris, Nathan, additional, and Buchner, David A., additional
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- 2017
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10. A chromosome 5q31.1 locus associates with tuberculin skin test reactivity in HIV-positive individuals from tuberculosis hyper-endemic regions in east Africa
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Sobota, Rafal S., primary, Stein, Catherine M., additional, Kodaman, Nuri, additional, Maro, Isaac, additional, Wieland-Alter, Wendy, additional, Igo, Robert P., additional, Magohe, Albert, additional, Malone, LaShaunda L., additional, Chervenak, Keith, additional, Hall, Noemi B., additional, Matee, Mecky, additional, Mayanja-Kizza, Harriet, additional, Joloba, Moses, additional, Moore, Jason H., additional, Scott, William K., additional, Lahey, Timothy, additional, Boom, W. Henry, additional, von Reyn, C. Fordham, additional, Williams, Scott M., additional, and Sirugo, Giorgio, additional
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- 2017
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11. The Great Migration and African-American Genomic Diversity
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Baharian, Soheil, primary, Barakatt, Maxime, additional, Gignoux, Christopher R., additional, Shringarpure, Suyash, additional, Errington, Jacob, additional, Blot, William J., additional, Bustamante, Carlos D., additional, Kenny, Eimear E., additional, Williams, Scott M., additional, Aldrich, Melinda C., additional, and Gravel, Simon, additional
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- 2016
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12. PLOS Genetics Data Sharing Policy: In Pursuit of Functional Utility
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Barsh, Gregory S., primary, Cooper, Gregory M., additional, Copenhaver, Gregory P., additional, Gibson, Greg, additional, McCarthy, Mark I., additional, Tang, Hua, additional, and Williams, Scott M., additional
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- 2015
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13. Pleiotropic Effects of Immune Responses Explain Variation in the Prevalence of Fibroproliferative Diseases
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Russell, Shirley B., primary, Smith, Joan C., additional, Huang, Minjun, additional, Trupin, Joel S., additional, and Williams, Scott M., additional
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- 2015
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14. Up For A Challenge (U4C): Stimulating innovation in breast cancer genetic epidemiology.
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null, null, Mechanic, Leah E., Dathe, Marina, Gillanders, Elizabeth M., Myers, Chad L., Wang, Wen, Ritchie, Marylyn D., Schildkraut, Joellen, Schumacher, Fredrick, Williams, Scott M., Lindström, Sara, Daily, Kenneth M., Sieberts, Solveig K., Amos, Christopher I., Chen, Huann-Sheng, Feuer, Eric J., Cox, Nancy J., Guertin, Michael J., Liu, Yunxian, and Hoffman, Joshua
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GENETICS of breast cancer ,CANCER risk factors - Abstract
The article focuses on the initiative "Up For A Challenge (U4C)—Stimulating Innovation in Breast Cancer Genetic Epidemiology" by the American organization National Cancer Institute (NCI). Topics discussed include understanding the role of disease risk through genome-wide association studies (GWAS) of the genetic variants of breast cancer, review by National Institutes of Health (NIH) of entries, and chart on U4C entries received.
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- 2017
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15. Recurrent Tissue-Specific mtDNA Mutations Are Common in Humans
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Samuels, David C., primary, Li, Chun, additional, Li, Bingshan, additional, Song, Zhuo, additional, Torstenson, Eric, additional, Boyd Clay, Hayley, additional, Rokas, Antonis, additional, Thornton-Wells, Tricia A., additional, Moore, Jason H., additional, Hughes, Tia M., additional, Hoffman, Robert D., additional, Haines, Jonathan L., additional, Murdock, Deborah G., additional, Mortlock, Douglas P., additional, and Williams, Scott M., additional
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- 2013
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16. Guidelines for Genome-Wide Association Studies
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Barsh, Gregory S., primary, Copenhaver, Gregory P., additional, Gibson, Greg, additional, and Williams, Scott M., additional
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- 2012
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17. The Association of the Vanin-1 N131S Variant with Blood Pressure Is Mediated by Endoplasmic Reticulum-Associated Degradation and Loss of Function.
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Wang, Ya-Juan, Tayo, Bamidele O., Bandyopadhyay, Anupam, Wang, Heming, Feng, Tao, Franceschini, Nora, Tang, Hua, Gao, Jianmin, Sung, Yun Ju, Elston, Robert C., Williams, Scott M., Cooper, Richard S., Mu, Ting-Wei, and Zhu, Xiaofeng
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HYPERTENSION genetics ,SINGLE nucleotide polymorphisms ,BLOOD pressure ,ENDOPLASMIC reticulum ,BLOOD plasma - Abstract
High blood pressure (BP) is the most common cardiovascular risk factor worldwide and a major contributor to heart disease and stroke. We previously discovered a BP-associated missense SNP (single nucleotide polymorphism)–rs2272996–in the gene encoding vanin-1, a glycosylphosphatidylinositol (GPI)-anchored membrane pantetheinase. In the present study, we first replicated the association of rs2272996 and BP traits with a total sample size of nearly 30,000 individuals from the Continental Origins and Genetic Epidemiology Network (COGENT) of African Americans (P = 0.01). This association was further validated using patient plasma samples; we observed that the N131S mutation is associated with significantly lower plasma vanin-1 protein levels. We observed that the N131S vanin-1 is subjected to rapid endoplasmic reticulum-associated degradation (ERAD) as the underlying mechanism for its reduction. Using HEK293 cells stably expressing vanin-1 variants, we showed that N131S vanin-1 was degraded significantly faster than wild type (WT) vanin-1. Consequently, there were only minimal quantities of variant vanin-1 present on the plasma membrane and greatly reduced pantetheinase activity. Application of MG-132, a proteasome inhibitor, resulted in accumulation of ubiquitinated variant protein. A further experiment demonstrated that atenolol and diltiazem, two current drugs for treating hypertension, reduce the vanin-1 protein level. Our study provides strong biological evidence for the association of the identified SNP with BP and suggests that vanin-1 misfolding and degradation are the underlying molecular mechanism. [ABSTRACT FROM AUTHOR]
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- 2014
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18. Cis-eQTL-based trans-ethnic meta-analysis reveals novel genes associated with breast cancer risk
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Noah Zaitlen, John S. Witte, Lancelote Leong, Michael N. Passarelli, Caroline G. Tai, Scott Huntsman, Joshua D. Hoffman, Nima C. Emami, Elad Ziv, Donglei Hu, Rebecca E. Graff, Arunabha Majumdar, Dexter Hadley, and Williams, Scott M
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0301 basic medicine ,Oncology ,Aging ,Cancer Research ,Physiology ,Gene Expression ,Genome-wide association study ,Disease ,QH426-470 ,Mathematical and Statistical Techniques ,0302 clinical medicine ,Risk Factors ,Breast Tumors ,Medicine and Health Sciences ,Ethnicity ,2.1 Biological and endogenous factors ,Breast ,Aetiology ,Genetics (clinical) ,Cancer ,GTPase-Activating Proteins ,Genomics ,Single Nucleotide ,Biobank ,Body Fluids ,3. Good health ,Blood ,030220 oncology & carcinogenesis ,Physical Sciences ,Female ,Anatomy ,Transcriptome Analysis ,Statistics (Mathematics) ,Research Article ,Biotechnology ,medicine.medical_specialty ,Quantitative Trait Loci ,Ethnic Groups ,Breast Neoplasms ,Single-nucleotide polymorphism ,Biology ,Research and Analysis Methods ,Polymorphism, Single Nucleotide ,03 medical and health sciences ,Breast cancer ,Internal medicine ,Breast Cancer ,Genome-Wide Association Studies ,medicine ,Genetics ,Humans ,Genetic Predisposition to Disease ,Statistical Methods ,Polymorphism ,Molecular Biology ,Ecology, Evolution, Behavior and Systematics ,Genetic association ,Human Genome ,Reproductive System ,Cancers and Neoplasms ,Biology and Life Sciences ,Computational Biology ,Membrane Proteins ,Human Genetics ,Genome Analysis ,Endonucleases ,medicine.disease ,030104 developmental biology ,Genetics of Disease ,Expression quantitative trait loci ,Carrier Proteins ,Transcriptome ,Breast Tissue ,Mathematics ,Meta-Analysis ,Genome-Wide Association Study ,Developmental Biology - Abstract
Breast cancer is the most common solid organ malignancy and the most frequent cause of cancer death among women worldwide. Previous research has yielded insights into its genetic etiology, but there remains a gap in the understanding of genetic factors that contribute to risk, and particularly in the biological mechanisms by which genetic variation modulates risk. The National Cancer Institute’s “Up for a Challenge” (U4C) competition provided an opportunity to further elucidate the genetic basis of the disease. Our group leveraged the seven datasets made available by the U4C organizers and data from the publicly available UK Biobank cohort to examine associations between imputed gene expression and breast cancer risk. In particular, we used reference datasets describing the breast tissue and whole blood transcriptomes to impute expression levels in breast cancer cases and controls. In trans-ethnic meta-analyses of U4C and UK Biobank data, we found significant associations between breast cancer risk and the expression of RCCD1 (joint p-value: 3.6x10-06) and DHODH (p-value: 7.1x10-06) in breast tissue, as well as a suggestive association for ANKLE1 (p-value: 9.3x10-05). Expression of RCCD1 in whole blood was also suggestively associated with disease risk (p-value: 1.2x10-05), as were expression of ACAP1 (p-value: 1.9x10-05) and LRRC25 (p-value: 5.2x10-05). While genome-wide association studies (GWAS) have implicated RCCD1 and ANKLE1 in breast cancer risk, they have not identified the remaining three genes. Among the genetic variants that contributed to the predicted expression of the five genes, we found 23 nominally (p-value < 0.05) associated with breast cancer risk, among which 15 are not in high linkage disequilibrium with risk variants previously identified by GWAS. In summary, we used a transcriptome-based approach to investigate the genetic underpinnings of breast carcinogenesis. This approach provided an avenue for deciphering the functional relevance of genes and genetic variants involved in breast cancer., Author summary There is a clear genetic basis of breast cancer, and previous work has identified numerous genetic variants that increase risk of this common disease. However, much of the underlying genetic variation in breast cancer remains unexplained. To address this void, as part of the National Cancer Institute’s “Up for a Challenge” (U4C) competition, we undertook a large-scale study of genetically regulated gene expression and breast cancer. Specifically, we estimated gene expression levels based on germline genetics for subjects in the seven breast cancer studies provided by U4C and for subjects in the UK Biobank. We then evaluated associations between gene expression and breast cancer and detected three novel and two known breast cancer genes. These genes exhibit potential biological mechanisms for impacting breast carcinogenesis. Our work highlights the value of leveraging different sources of data to more thoroughly study the genetic basis of complex diseases.
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- 2017
19. Population structure of Hispanics in the United States: the multi-ethnic study of atherosclerosis
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Jasmin Divers, Quenna Wong, Josyf C. Mychaleckyj, Mark O. Goodarzi, Kathleen F. Kerr, Kent D. Taylor, Stephen S. Rich, Carmen A. Peralta, Jerome I. Rotter, Xiuqing Guo, Ana V. Diez-Roux, Michèle M. Sale, Ani Manichaikul, Carlos J. Rodriguez, Walter Palmas, Michael Y. Tsai, Wei-Min Chen, Kayleen Williams, and Williams, Scott M
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Cancer Research ,Linkage disequilibrium ,Population genetics ,Genome-wide association study ,030204 cardiovascular system & hematology ,Cardiovascular ,0302 clinical medicine ,Indians ,Cluster Analysis ,International HapMap Project ,Genetics (clinical) ,African Continental Ancestry Group ,0303 health sciences ,education.field_of_study ,Intracellular Signaling Peptides and Proteins ,Single Nucleotide ,Hispanic or Latino ,Blacks ,Protein-Serine-Threonine Kinases ,Hispanic Americans ,North American ,Research Article ,lcsh:QH426-470 ,European Continental Ancestry Group ,Population ,Black People ,Single-nucleotide polymorphism ,HapMap Project ,Biology ,Protein Serine-Threonine Kinases ,Polymorphism, Single Nucleotide ,White People ,03 medical and health sciences ,Population Groups ,Clinical Research ,Genome-Wide Association Studies ,Genetics ,Humans ,Polymorphism ,education ,Molecular Biology ,Ecology, Evolution, Behavior and Systematics ,Triglycerides ,Genetic Association Studies ,030304 developmental biology ,Genetic association ,Genetic heterogeneity ,Whites ,Human Genome ,Human Genetics ,Atherosclerosis ,United States ,Lipoprotein Lipase ,lcsh:Genetics ,Indians, North American ,Demography ,Developmental Biology - Abstract
Using ∼60,000 SNPs selected for minimal linkage disequilibrium, we perform population structure analysis of 1,374 unrelated Hispanic individuals from the Multi-Ethnic Study of Atherosclerosis (MESA), with self-identification corresponding to Central America (n = 93), Cuba (n = 50), the Dominican Republic (n = 203), Mexico (n = 708), Puerto Rico (n = 192), and South America (n = 111). By projection of principal components (PCs) of ancestry to samples from the HapMap phase III and the Human Genome Diversity Panel (HGDP), we show the first two PCs quantify the Caucasian, African, and Native American origins, while the third and fourth PCs bring out an axis that aligns with known South-to-North geographic location of HGDP Native American samples and further separates MESA Mexican versus Central/South American samples along the same axis. Using k-means clustering computed from the first four PCs, we define four subgroups of the MESA Hispanic cohort that show close agreement with self-identification, labeling the clusters as primarily Dominican/Cuban, Mexican, Central/South American, and Puerto Rican. To demonstrate our recommendations for genetic analysis in the MESA Hispanic cohort, we present pooled and stratified association analysis of triglycerides for selected SNPs in the LPL and TRIB1 gene regions, previously reported in GWAS of triglycerides in Caucasians but as yet unconfirmed in Hispanic populations. We report statistically significant evidence for genetic association in both genes, and we further demonstrate the importance of considering population substructure and genetic heterogeneity in genetic association studies performed in the United States Hispanic population., Author Summary Using genotype data from about 60,000 distinct genetic markers, we examined population structure in 1,374 unrelated Hispanic individuals from the Multi-Ethnic Study of Atherosclerosis (MESA), with self-identification corresponding to Central America (n = 93), Cuba (n = 50), the Dominican Republic (n = 203), Mexico (n = 708), Puerto Rico (n = 192), and South America (n = 111). By comparing genetic ancestry of MESA Hispanic participants to reference samples representing worldwide diversity, we show major differences in ancestry of MESA Hispanics reflecting their Caucasian, African, and Native American origins, with finer differences corresponding to North-South geographic origins that separate MESA Mexican versus Central/South American samples. Based on our analysis, we define four subgroups of the MESA Hispanic cohort that show close agreement with the following self-identified regions of origin: Dominican/Cuban, Mexican, Central/South American, and Puerto Rican. We examine association of triglycerides with selected genetic markers, and we further demonstrate the importance of considering differences in genetic ancestry (or factors associated with genetic ancestry) when performing genetic studies of the United States Hispanic population.
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- 2012
20. Correction: Whole exome sequencing reveals HSPA1L as a genetic risk factor for spontaneous preterm birth.
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Huusko JM, Karjalainen MK, Graham BE, Zhang G, Farrow EG, Miller NA, Jacobsson B, Eidem HR, Murray JC, Bedell B, Breheny P, Brown NW, Bødker FL, Litterman NK, Jiang PP, Russell L, Hinds DA, Hu Y, Rokas A, Teramo K, Christensen K, Williams SM, Rämet M, Kingsmore SF, Ryckman KK, Hallman M, and Muglia LJ
- Abstract
[This corrects the article DOI: 10.1371/journal.pgen.1007394.].
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- 2018
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21. Up For A Challenge (U4C): Stimulating innovation in breast cancer genetic epidemiology.
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Mechanic LE, Lindström S, Daily KM, Sieberts SK, Amos CI, Chen HS, Cox NJ, Dathe M, Feuer EJ, Guertin MJ, Hoffman J, Liu Y, Moore JH, Myers CL, Ritchie MD, Schildkraut J, Schumacher F, Witte JS, Wang W, Williams SM, and Gillanders EM
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- Breast Neoplasms epidemiology, Female, Genome-Wide Association Study statistics & numerical data, Genome-Wide Association Study trends, Humans, Inventions, Research Report, Breast Neoplasms genetics, Genome-Wide Association Study methods
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- 2017
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22. Admixture mapping in lupus identifies multiple functional variants within IFIH1 associated with apoptosis, inflammation, and autoantibody production.
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Molineros JE, Maiti AK, Sun C, Looger LL, Han S, Kim-Howard X, Glenn S, Adler A, Kelly JA, Niewold TB, Gilkeson GS, Brown EE, Alarcón GS, Edberg JC, Petri M, Ramsey-Goldman R, Reveille JD, Vilá LM, Freedman BI, Tsao BP, Criswell LA, Jacob CO, Moore JH, Vyse TJ, Langefeld CL, Guthridge JM, Gaffney PM, Moser KL, Scofield RH, Alarcón-Riquelme ME, Williams SM, Merrill JT, James JA, Kaufman KM, Kimberly RP, Harley JB, and Nath SK
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- Alleles, Antigens, Nuclear genetics, Antigens, Nuclear immunology, Apoptosis genetics, Autoantibodies genetics, Autoantibodies immunology, Chromosome Mapping, DNA-Binding Proteins genetics, DNA-Binding Proteins immunology, Genetic Predisposition to Disease, Genome, Human, Haplotypes, Humans, Inflammation genetics, Interferon-Induced Helicase, IFIH1, Ku Autoantigen, Lupus Erythematosus, Systemic immunology, Polymorphism, Single Nucleotide, Protein Binding, White People genetics, Black or African American genetics, DEAD-box RNA Helicases genetics, Lupus Erythematosus, Systemic genetics
- Abstract
Systemic lupus erythematosus (SLE) is an inflammatory autoimmune disease with a strong genetic component. African-Americans (AA) are at increased risk of SLE, but the genetic basis of this risk is largely unknown. To identify causal variants in SLE loci in AA, we performed admixture mapping followed by fine mapping in AA and European-Americans (EA). Through genome-wide admixture mapping in AA, we identified a strong SLE susceptibility locus at 2q22-24 (LOD=6.28), and the admixture signal is associated with the European ancestry (ancestry risk ratio ~1.5). Large-scale genotypic analysis on 19,726 individuals of African and European ancestry revealed three independently associated variants in the IFIH1 gene: an intronic variant, rs13023380 [P(meta) = 5.20×10(-14); odds ratio, 95% confidence interval = 0.82 (0.78-0.87)], and two missense variants, rs1990760 (Ala946Thr) [P(meta) = 3.08×10(-7); 0.88 (0.84-0.93)] and rs10930046 (Arg460His) [P(dom) = 1.16×10(-8); 0.70 (0.62-0.79)]. Both missense variants produced dramatic phenotypic changes in apoptosis and inflammation-related gene expression. We experimentally validated function of the intronic SNP by DNA electrophoresis, protein identification, and in vitro protein binding assays. DNA carrying the intronic risk allele rs13023380 showed reduced binding efficiency to a cellular protein complex including nucleolin and lupus autoantigen Ku70/80, and showed reduced transcriptional activity in vivo. Thus, in SLE patients, genetic susceptibility could create a biochemical imbalance that dysregulates nucleolin, Ku70/80, or other nucleic acid regulatory proteins. This could promote antibody hypermutation and auto-antibody generation, further destabilizing the cellular network. Together with molecular modeling, our results establish a distinct role for IFIH1 in apoptosis, inflammation, and autoantibody production, and explain the molecular basis of these three risk alleles for SLE pathogenesis., Competing Interests: The authors have declared that no competing interests exist.
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- 2013
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