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4 results on '"Chris Haiman"'

1. Methylation patterns associated with C-reactive protein in racially and ethnically diverse populations

Author

Jessica I. Lundin, Ulrike Peters, Yao Hu, Farah Ammous, Christy L. Avery, Emelia J. Benjamin, Joshua C. Bis, Jennifer A. Brody, Chris Carlson, Mary Cushman, Chris Gignoux, Xiuqing Guo, Jeff Haessler, Chris Haiman, Roby Joehanes, Silva Kasela, Eimear Kenny, Tuuli Lapalainien, Daniel Levy, Chunyu Liu, Yongmei Liu, Ruth J.F. Loos, Ake Lu, Tara Matise, Kari E. North, Sungshim L. Park, Scott M. Ratliff, Alex Reiner, Stephen S. Rich, Jerome I. Rotter, Jennifer A. Smith, Nona Sotoodehnia, Russell Tracy, David Van den Berg, Huichun Xu, Ting Ye, Wei Zhao, Laura M. Raffield, and Charles Kooperberg

Subjects
Inflammation, C-reactive protein, methylation, epigenetics, EWAS, racial and ethnic diversity, Genetics, QH426-470
Abstract

ABSTRACTSystemic low-grade inflammation is a feature of chronic disease. C-reactive protein (CRP) is a common biomarker of inflammation and used as an indicator of disease risk; however, the role of inflammation in disease is not completely understood. Methylation is an epigenetic modification in the DNA which plays a pivotal role in gene expression. In this study we evaluated differential DNA methylation patterns associated with blood CRP level to elucidate biological pathways and genetic regulatory mechanisms to improve the understanding of chronic inflammation. The racially and ethnically diverse participants in this study were included as 50% White, 41% Black or African American, 7% Hispanic or Latino/a, and 2% Native Hawaiian, Asian American, American Indian, or Alaska Native (total n = 13,433) individuals. We replicated 113 CpG sites from 87 unique loci, of which five were novel (CADM3, NALCN, NLRC5, ZNF792, and cg03282312), across a discovery set of 1,150 CpG sites associated with CRP level (p

Published
2024
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2. Minority-centric meta-analyses of blood lipid levels identify novel loci in the Population Architecture using Genomics and Epidemiology (PAGE) study.

Author

Yao Hu, Mariaelisa Graff, Jeffrey Haessler, Steven Buyske, Stephanie A Bien, Ran Tao, Heather M Highland, Katherine K Nishimura, Niha Zubair, Yingchang Lu, Marie Verbanck, Austin T Hilliard, Derek Klarin, Scott M Damrauer, Yuk-Lam Ho, VA Million Veteran Program, Peter W F Wilson, Kyong-Mi Chang, Philip S Tsao, Kelly Cho, Christopher J O'Donnell, Themistocles L Assimes, Lauren E Petty, Jennifer E Below, Ozan Dikilitas, Daniel J Schaid, Matthew L Kosel, Iftikhar J Kullo, Laura J Rasmussen-Torvik, Gail P Jarvik, Qiping Feng, Wei-Qi Wei, Eric B Larson, Frank D Mentch, Berta Almoguera, Patrick M Sleiman, Laura M Raffield, Adolfo Correa, Lisa W Martin, Martha Daviglus, Tara C Matise, Jose Luis Ambite, Christopher S Carlson, Ron Do, Ruth J F Loos, Lynne R Wilkens, Loic Le Marchand, Chris Haiman, Daniel O Stram, Lucia A Hindorff, Kari E North, Charles Kooperberg, Iona Cheng, and Ulrike Peters

Subjects
Genetics, QH426-470
Abstract

Lipid levels are important markers for the development of cardio-metabolic diseases. Although hundreds of associated loci have been identified through genetic association studies, the contribution of genetic factors to variation in lipids is not fully understood, particularly in U.S. minority groups. We performed genome-wide association analyses for four lipid traits in over 45,000 ancestrally diverse participants from the Population Architecture using Genomics and Epidemiology (PAGE) Study, followed by a meta-analysis with several European ancestry studies. We identified nine novel lipid loci, five of which showed evidence of replication in independent studies. Furthermore, we discovered one novel gene in a PrediXcan analysis, minority-specific independent signals at eight previously reported loci, and potential functional variants at two known loci through fine-mapping. Systematic examination of known lipid loci revealed smaller effect estimates in African American and Hispanic ancestry populations than those in Europeans, and better performance of polygenic risk scores based on minority-specific effect estimates. Our findings provide new insight into the genetic architecture of lipid traits and highlight the importance of conducting genetic studies in diverse populations in the era of precision medicine.

Published
2020
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3. Abstract 1954: Black-White differences in prospective serum metabolites and biochemical pathways associated with prostate cancer risk in a COMETS consortium project

Author

Jungeun Lim, Grace Hong, Tracy M. Layne, Chris Haiman, Loic Le Marchand, Stephanie J. Weinstein, Jiaqi Huang, and Demetrius Albanes

Subjects
Cancer Research, Oncology
Abstract

Prostate cancer incidence and mortality rates are substantially higher in Black men as compared with White men. It is unclear which exposures and biochemical pathways may explain this racial disparity. We examined the metabolomic profiles of prostate cancer risk by race within a subset of studies from the COnsortium of METabolomics Studies (COMETS). A meta-analysis of six cohort-based studies including 1,769 prostate cancer case-control sets and 831 serum metabolites was conducted using the multivariable logistic regression and random effects models. Overall, 11 metabolites were significantly associated with prostate cancer risk, including L-cystine (1-SD OR=0.77; P=0.009) and biliverdin (1-SD OR=1.12; P=0.017). The race-stratified analysis of chemical classes revealed that lipids were positively associated with prostate cancer risk only in White men, whereas amino acids were associated inversely primarily in Black men. The latter included metabolites related to tryptophan, lysine, and phenylalanine metabolism; e.g., the strongest metabolite being alpha-N-phenylacetyl-L-glutamine (1-SD OR=0.81; P=0.003), which is produced by Clostridial anaerobic bacteria in the gut. Lipids related to fatty acid metabolism were associated with higher prostate cancer risk in both Black and White men (e.g., docosahexaenoylcholine and 3-hydroxybutyroylglycine), and alpha-tocopherol was inversely associated in White men (1-SD OR=0.69; P=0.011). For other races combined, N-acetyltryptophan (1-SD OR=0.04; P=0.025) showed the strongest metabolite-risk association. To our knowledge, this is the first metabolomic meta-analysis of prostate cancer risk which provides evidence of biochemical etiologic differences relevant to the Black-White disease disparity. Table 1. Race-stratified meta-analysis estimates of prostate cancer risk by chemical class a White participants Chemical class # Metabolites P-value OR (95% CI) I2 (%) Amino acids 188 0.226 1.005 (0.997-1.013) 15.7 Carbohydrates 24 0.495 1.003 (0.994-1.012) 0.0 Cofactors and vitamins 30 0.442 0.998 (0.991-1.004) 0.0 Energy metabolites 11 0.843 0.991 (0.906-1.084) 34.1 Lipids 339 Citation Format: Jungeun Lim, Grace Hong, Tracy M. Layne, Chris Haiman, Loic Le Marchand, Stephanie J. Weinstein, Jiaqi Huang, Demetrius Albanes. Black-White differences in prospective serum metabolites and biochemical pathways associated with prostate cancer risk in a COMETS consortium project [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 1954.

Published
2023

4. Identification of a common variant with potential pleiotropic effect on risk of inflammatory bowel disease and colorectal cancer

Author

Hamed Khalili, Jian Gong, Hermann Brenner, Thomas R. Austin, Carolyn M. Hutter, Yoshifumi Baba, John A. Baron, Sonja I. Berndt, Stéphane Bézieau, Bette Caan, Peter T. Campbell, Jenny Chang-Claude, Stephen J. Chanock, Constance Chen, Li Hsu, Shuo Jiao, David V. Conti, David Duggan, Charles S. Fuchs, Manish Gala, Steven Gallinger, Robert W. Haile, Tabitha A. Harrison, Richard Hayes, Aditi Hazra, Brian Henderson, Chris Haiman, Michael Hoffmeister, John L. Hopper, Mark A. Jenkins, Laurence N. Kolonel, Sébastien Küry, Andrea LaCroix, Loic Le Marchand, Mathieu Lemire, Noralane M. Lindor, Jing Ma, JoAnn E. Manson, Teppei Morikawa, Hongmei Nan, Kimmie Ng, Polly A. Newcomb, Reiko Nishihara, John D. Potter, Conghui Qu, Robert E. Schoen, Fredrick R. Schumacher, Daniela Seminara, Darin Taverna, Stephen Thibodeau, Jean Wactawski-Wende, Emily White, Kana Wu, Brent W. Zanke, Graham Casey, Thomas J. Hudson, Peter Kraft, Ulrike Peters, Martha L. Slattery, Shuji Ogino, and Andrew T. Chan

Subjects
Risk, Oncology, Cancer Research, medicine.medical_specialty, Colorectal cancer, Original Manuscript, Single-nucleotide polymorphism, Genome-wide association study, Biology, Bioinformatics, Polymorphism, Single Nucleotide, Inflammatory bowel disease, White People, Crohn Disease, Gene Frequency, Internal medicine, medicine, Humans, Genetic Predisposition to Disease, Oncology & Carcinogenesis, neoplasms, Allele frequency, Oncology And Carcinogenesis, Cancer, General Medicine, Odds ratio, medicine.disease, digestive system diseases, Minor allele frequency, Colitis, Ulcerative, Microsatellite Instability, Colorectal Neoplasms, Genome-Wide Association Study, Microsatellite Repeats
Abstract

Although genome-wide association studies (GWAS) have separately identified many genetic susceptibility loci for ulcerative colitis (UC), Crohn's disease (CD) and colorectal cancer (CRC), there has been no large-scale examination for pleiotropy, or shared genetic susceptibility, for these conditions. We used logistic regression modeling to examine the associations of 181 UC and CD susceptibility variants previously identified by GWAS with risk of CRC using data from the Genetics and Epidemiology of Colorectal Cancer Consortium and the Colon Cancer Family Registry. We also examined associations of significant variants with clinical and molecular characteristics in a subset of the studies. Among 11794 CRC cases and 14190 controls, rs11676348, the susceptibility single nucleotide polymorphism (SNP) for UC, was significantly associated with reduced risk of CRC (P = 7E-05). The multivariate-adjusted odds ratio of CRC with each copy of the T allele was 0.93 (95% CI 0.89-0.96). The association of the SNP with risk of CRC differed according to mucinous histological features (P heterogeneity = 0.008). In addition, the (T) allele was associated with lower risk of tumors with Crohn's-like reaction but not tumors without such immune infiltrate (P heterogeneity = 0.02) and microsatellite instability-high (MSI-high) but not microsatellite stable or MSI-low tumors (P heterogeneity = 0.03). The minor allele (T) in SNP rs11676348, located downstream from CXCR2 that has been implicated in CRC progression, is associated with a lower risk of CRC, particularly tumors with a mucinous component, Crohn's-like reaction and MSI-high. Our findings offer the promise of risk stratification of inflammatory bowel disease patients for complications such as CRC.

Published
2015

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