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Crohn Disease: HELP
Articles by Ming-Hsi Wang
Based on 7 articles published since 2010
(Why 7 articles?)
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Between 2010 and 2020, Ming-Hsi Wang wrote the following 7 articles about Crohn Disease.
 
+ Citations + Abstracts
1 Review Crohn's Disease: Genetics Update. 2017

Wang, Ming-Hsi / Picco, Michael F. ·Department of Gastroenterology and Hepatology, Mayo Clinic Jacksonville, 4500 San Pablo Road, Jacksonville, FL 32224, USA. Electronic address: Wang.Ming-Hsi@mayo.edu. · Department of Gastroenterology and Hepatology, Mayo Clinic Jacksonville, 4500 San Pablo Road, Jacksonville, FL 32224, USA. ·Gastroenterol Clin North Am · Pubmed #28838408.

ABSTRACT: Since the discovery of the first Crohn's disease (CD) gene NOD2 in 2001, 140 genetic loci have been found in whites using high-throughput genome-wide association studies. Several genes influence the CD subphenotypes and treatment response. With the observations of increasing prevalence in Asia and developing countries and the incomplete explanation of CD variance, other underexplored areas need to be integrated through novel methodologies. Algorithms that incorporate specific genetic risk alleles with other biomarkers will be developed and used to predict CD disease course, complications, and response to specific therapies, allowing precision medicine to become real in CD.

2 Article Nonsteroidal anti-inflammatory drug-induced protein-losing enteropathy: a great masquerade of Crohn's disease. 2017

Vinsard, Daniela Guerrero / Stark, Mark E / Lewis, Jason T / Wang, Ming-Hsi. ·Division of Gastroenterology and Hepatology, Mayo Clinic, Jacksonville, Florida, USA. ·Gastrointest Endosc · Pubmed #28554654.

ABSTRACT: -- No abstract --

3 Article Genome-Wide Association Study Identifies African-Specific Susceptibility Loci in African Americans With Inflammatory Bowel Disease. 2017

Brant, Steven R / Okou, David T / Simpson, Claire L / Cutler, David J / Haritunians, Talin / Bradfield, Jonathan P / Chopra, Pankaj / Prince, Jarod / Begum, Ferdouse / Kumar, Archana / Huang, Chengrui / Venkateswaran, Suresh / Datta, Lisa W / Wei, Zhi / Thomas, Kelly / Herrinton, Lisa J / Klapproth, Jan-Micheal A / Quiros, Antonio J / Seminerio, Jenifer / Liu, Zhenqiu / Alexander, Jonathan S / Baldassano, Robert N / Dudley-Brown, Sharon / Cross, Raymond K / Dassopoulos, Themistocles / Denson, Lee A / Dhere, Tanvi A / Dryden, Gerald W / Hanson, John S / Hou, Jason K / Hussain, Sunny Z / Hyams, Jeffrey S / Isaacs, Kim L / Kader, Howard / Kappelman, Michael D / Katz, Jeffry / Kellermayer, Richard / Kirschner, Barbara S / Kuemmerle, John F / Kwon, John H / Lazarev, Mark / Li, Ellen / Mack, David / Mannon, Peter / Moulton, Dedrick E / Newberry, Rodney D / Osuntokun, Bankole O / Patel, Ashish S / Saeed, Shehzad A / Targan, Stephan R / Valentine, John F / Wang, Ming-Hsi / Zonca, Martin / Rioux, John D / Duerr, Richard H / Silverberg, Mark S / Cho, Judy H / Hakonarson, Hakon / Zwick, Michael E / McGovern, Dermot P B / Kugathasan, Subra. ·Department of Medicine, Meyerhoff Inflammatory Bowel Disease Center, Johns Hopkins University School of Medicine, Baltimore, Maryland; Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland. · Department of Pediatrics, Emory University School of Medicine, Atlanta, Georgia. · Department of Genetics, Genomics and Informatics, University of Tennessee Health Science Center, Memphis, Tennessee; Computational and Statistical Genomics Branch, National Human Genome Research Institute, National Institutes of Health, Baltimore, Maryland. · Department of Human Genetics, Emory University School of Medicine, Atlanta, Georgia. · F. Widjaja Foundation Inflammatory Bowel and Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles, California. · Center for Applied Genomics, Abramson Research Center, The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania. · Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland. · Department of Medicine, Meyerhoff Inflammatory Bowel Disease Center, Johns Hopkins University School of Medicine, Baltimore, Maryland. · Kaiser Permanente, Oakland, California. · University of Pennsylvania, Philadelphia, Pennsylvania. · Department of Pediatrics, Medical University of South Carolina, Pediatric Center for Inflammatory Bowel Disorders, Summerville, South Carolina. · Department of Gastroenterology, Medical University of South Carolina Digestive Disease Center, Charleston, South Carolina. · Department of Molecular and Cellular Physiology, Louisiana State University Health Sciences Center, Shreveport, Louisiana. · Department of Pediatrics, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania. · Department of Medicine, Johns Hopkins University Schools of Medicine & Nursing, Baltimore, Maryland. · Department of Medicine, University of Maryland School of Medicine, Baltimore, Maryland. · Department of Medicine, Washington University School of Medicine, St Louis, Missouri. · Division of Gastroenterology, Hepatology and Nutrition, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio. · Department of Medicine, Emory University School of Medicine, Atlanta, Georgia. · Department of Medicine, University of Louisville, Louisville, Kentucky. · Charlotte Gastroenterology and Hepatology, Charlotte, North Carolina. · Department of Medicine, Baylor College of Medicine; Veterans Affairs Health Services Research and Development Service, Center for Innovations in Quality Effectiveness and Safety; Michael E. DeBakey Veterans Affairs Medical Center, Houston, Texas. · Department of Pediatrics, Willis-Knighton Physician Network, Shreveport, Louisiana. · Connecticut Children's Medical Center, Hartford, Connecticut. · Department of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina. · Department of Pediatrics, University of Maryland School of Medicine, Baltimore, Maryland. · Department of Pediatrics, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina. · Case Western Reserve University, Cleveland, Ohio. · Section of Pediatric Gastroenterology, Baylor College of Medicine, Texas Children's Hospital, Houston, Texas. · Department of Pediatrics, University of Chicago Comer Children's Hospital, Chicago, Illinois. · Medicine and Physiology and Biophysics, Medical College of Virginia Campus of Virginia Commonwealth University, Richmond, Virginia. · Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas. · Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland. · Department of Medicine, Stony Brook University School of Medicine, Stony Brook, New York. · Department of Pediatrics, University of Ottawa and Children's Hospital of Eastern Ontario, Ottawa, Ontario, Canada. · Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama. · Vanderbilt Children's Hospital, Nashville, Tennessee. · Department of Internal Medicine, Washington University School of Medicine, St Louis, Missouri. · Department of Pediatrics, Cook Children's Medical Center, Fort Worth, Texas. · Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, Texas. · University of Utah, Health Sciences, Salt Lake City, Utah. · Division of Gastroenterology and Hepatology, Mayo Clinic Florida, Jacksonville, Florida. · Department of Internal Medicine, Henry Ford Health System, Detroit, Michigan. · Department of Medicine, Université de Montréal and the Montreal Heart Institute Research Center, Montreal, Quebec, Canada. · Department of Medicine and Clinical and Translational Science Institute, School of Medicine and Department of Human Genetics, Graduate School of Public Health; University of Pittsburgh, Pittsburgh, Pennsylvania. · Department of Medicine, Zane Cohen Centre for Digestive Diseases, Mount Sinai Hospital, University of Toronto, Toronto, Toronto, Ontario, Canada. · Medicine and Genetics, Icahn School of Medicine at Mount Sinai, Charles Bronfman Institute for Personalized Medicine, New York, New York. · Department of Pediatrics, Emory University School of Medicine, Atlanta, Georgia; Department of Human Genetics, Emory University School of Medicine, Atlanta, Georgia. Electronic address: skugath@emory.edu. ·Gastroenterology · Pubmed #27693347.

ABSTRACT: BACKGROUND & AIMS: The inflammatory bowel diseases (IBD) ulcerative colitis (UC) and Crohn's disease (CD) cause significant morbidity and are increasing in prevalence among all populations, including African Americans. More than 200 susceptibility loci have been identified in populations of predominantly European ancestry, but few loci have been associated with IBD in other ethnicities. METHODS: We performed 2 high-density, genome-wide scans comprising 2345 cases of African Americans with IBD (1646 with CD, 583 with UC, and 116 inflammatory bowel disease unclassified) and 5002 individuals without IBD (controls, identified from the Health Retirement Study and Kaiser Permanente database). Single-nucleotide polymorphisms (SNPs) associated at P < 5.0 × 10 RESULTS: We detected SNPs at HLA-DRB1, and African-specific SNPs at ZNF649 and LSAMP, with associations of genome-wide significance for UC. We detected SNPs at USP25 with associations of genome-wide significance for IBD. No associations of genome-wide significance were detected for CD. In addition, 9 genes previously associated with IBD contained SNPs with significant evidence for replication (P < 1.6 × 10 CONCLUSIONS: We performed a genome-wide association study of African Americans with IBD and identified loci associated with UC in only this population; we also replicated IBD, CD, and UC loci identified in European populations. The detection of variants associated with IBD risk in only people of African descent demonstrates the importance of studying the genetics of IBD and other complex diseases in populations beyond those of European ancestry.

4 Article Adenocarcinoma Arising From the Tip of the J-Pouch With Medically Refractory Crohn's Disease. 2016

Chen, Wei-Chung / Nassar, Aziza / Wang, Ming-Hsi. ·Division of Gastroenterology and Hepatology, Mayo Clinic, Jacksonville, Florida. · Department of Laboratory Medicine and Pathology, Mayo Clinic, Jacksonville, Florida. ·Clin Gastroenterol Hepatol · Pubmed #26898651.

ABSTRACT: -- No abstract --

5 Article Characterization of genetic loci that affect susceptibility to inflammatory bowel diseases in African Americans. 2015

Huang, Chengrui / Haritunians, Talin / Okou, David T / Cutler, David J / Zwick, Michael E / Taylor, Kent D / Datta, Lisa W / Maranville, Joseph C / Liu, Zhenqiu / Ellis, Shannon / Chopra, Pankaj / Alexander, Jonathan S / Baldassano, Robert N / Cross, Raymond K / Dassopoulos, Themistocles / Dhere, Tanvi A / Duerr, Richard H / Hanson, John S / Hou, Jason K / Hussain, Sunny Z / Isaacs, Kim L / Kachelries, Kelly E / Kader, Howard / Kappelman, Michael D / Katz, Jeffrey / Kellermayer, Richard / Kirschner, Barbara S / Kuemmerle, John F / Kumar, Archana / Kwon, John H / Lazarev, Mark / Mannon, Peter / Moulton, Dedrick E / Osuntokun, Bankole O / Patel, Ashish / Rioux, John D / Rotter, Jerome I / Saeed, Shehzad / Scherl, Ellen J / Silverberg, Mark S / Silverman, Ann / Targan, Stephan R / Valentine, John F / Wang, Ming-Hsi / Simpson, Claire L / Bridges, S Louis / Kimberly, Robert P / Rich, Stephen S / Cho, Judy H / Rienzo, Anna Di / Kao, Linda W H / McGovern, Dermot P B / Brant, Steven R / Kugathasan, Subra. ·Department of Epidemiology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD 21231, USA. · F. Widjaja Foundation Inflammatory Bowel and Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA 90049, USA. · Department of Pediatrics, Emory University School of Medicine, Atlanta, GA 30322, USA. · Department of Human Genetics, Emory University School of Medicine, Atlanta, GA 30322, USA. · Institute for Translational Genomics and Population Sciences and Division of Genomic Outcomes, Departments of Pediatrics and Medicine, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, CA,90502, USA. · Meyerhoff Inflammatory Bowel Disease Center, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA. · Committee on Clinical Pharmacology and Pharmacogenomics, and the Department of Human Genetics, The University of Chicago, Chicago, IL 60637, USA. · Department of Molecular and Cellular Physiology, Louisiana State University Health Sciences Center, Shreveport, LA 71130, USA. · Division of Gastroenterology and Nutrition, Children's Hospital of Philadelphia, Philadelphia, PA 19104, USA. · Division of Gastroenterology, University of Maryland, Baltimore, MD 21201, USA. · Department of Medicine, Washington University School of Medicine, St Louis, MO 63110, USA. · Department of Medicine, Emory University School of Medicine, Atlanta, GA 30322, USA. · Division of Gastroenterology, Hepatology and Nutrition, Department of Medicine, University of Pittsburgh School of Medicine, and Department of Human Genetics, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA 15261, USA. · Charlotte Gastroenterology and Hepatology, PLLC, Charlotte, NC 28207, USA. · Department of Medicine, Baylor College of Medicine; VA HSR&D Center for Innovations in Quality, Effectiveness and Safety , Michael E. DeBakey VA Medical Center, Houston, TX 77030, USA. · Department of Pediatrics, Willis-Knighton Physician Network, Shreveport, LA 71118, USA. · Division of Gastroenterology and Hepatology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27514, USA. · Department of Pediatrics, University of Maryland School of Medicine, Baltimore, MD 21201, USA. · Department of Pediatrics, University of North Carolina at Chapel Hill, Chapel Hill, NC 27514, USA. · Division of Gastroenterology, Case Western Reserve University, Cleveland, OH 44106, USA. · Section of Pediatric Gastroenterology, Baylor College of Medicine, Houston, TX, 77030. · Department of Pediatrics, University of Chicago Comer Children's Hospital, Chicago, IL 60637, USA. · Departments of Medicine and Physiology and Biophysics, VCU Program in Enteric Neuromuscular Sciences, Medical College of Virginia Campus of Virginia Commonwealth University, Richmond VA 23298, USA. · Section of Gastroenterology, Department of Medicine, University of Chicago, Chicago, IL 60637, USA. · Department of Medicine, University of Alabama at Birmingham, Birmingham, AL 35294, USA. · Division of Gastroenterology, Vanderbilt Children's Hospital, Nashville TN 37212, USA. · Department of Pediatrics, Cook Children's Medical Center, Fort Worth, TX 76104, USA. · Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. · Universite de Montreal and the Montreal Heart Institute, Research Center, Montreal, Quebec H1T 1C8, Canada. · Division of Gastroenterology, Hepatology and Nutrition, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA. · Department of Medicine, Weill Cornell Medical College, New York, NY 10065, USA. · Departments of Medicine, Surgery, Public Health Sciences, Immunology, and Molecular and Medical Genetics, University of Toronto, Samuel Lunenfeld Research Institute and Mount Sinai Hospital, Toronto General Hospital Research Institute, Toronto, Ontario M5S 2J7, Canada. · Department of Gastroenterology, Henry Ford Health System Detroit, MI 48208, USA. · Division of Gastroenterology, Hepatology and Nutrition, University of Utah, Salt Lake City, Utah. · Statistical Genetics Section, Inherited Disease Research Branch, National Human Genome Research Institute, National Institutes of Health, Baltimore, MD 21224, USA. · Division of Clinical Immunology & Rheumatology, University of Alabama at Birmingham, Birmingham, AL 35294, USA. · Center for Public Health Genomics, University of Virginia School of Medicine, Charlottesville, VA 22908, USA. · Department of Medicine and Genetics, Yale University, New Haven, CT 06520, USA. ·Gastroenterology · Pubmed #26278503.

ABSTRACT: BACKGROUND & AIMS: Inflammatory bowel disease (IBD) has familial aggregation in African Americans (AAs), but little is known about the molecular genetic susceptibility. Mapping studies using the Immunochip genotyping array expand the number of susceptibility loci for IBD in Caucasians to 163, but the contribution of the 163 loci and European admixture to IBD risk in AAs is unclear. We performed a genetic mapping study using the Immunochip to determine whether IBD susceptibility loci in Caucasians also affect risk in AAs and identify new associated loci. METHODS: We recruited AAs with IBD and without IBD (controls) from 34 IBD centers in the United States; additional controls were collected from 4 other Immunochip studies. Association and admixture loci were mapped for 1088 patients with Crohn's disease, 361 with ulcerative colitis, 62 with IBD type unknown, and 1797 controls; 130,241 autosomal single-nucleotide polymorphisms (SNPs) were analyzed. RESULTS: The strongest associations were observed between ulcerative colitis and HLA rs9271366 (P = 7.5 × 10(-6)), Crohn's disease and 5p13.1 rs4286721 (P = 3.5 × 10(-6)), and IBD and KAT2A rs730086 (P = 2.3 × 10(-6)). Additional suggestive associations (P < 4.2 × 10(-5)) were observed between Crohn's disease and IBD and African-specific SNPs in STAT5A and STAT3; between IBD and SNPs in IL23R, IL12B, and C2orf43; and between ulcerative colitis and SNPs near HDAC11 and near LINC00994. The latter 3 loci have not been previously associated with IBD, but require replication. Established Caucasian associations were replicated in AAs (P < 3.1 × 10(-4)) at NOD2, IL23R, 5p15.3, and IKZF3. Significant admixture (P < 3.9 × 10(-4)) was observed for 17q12-17q21.31 (IZKF3 through STAT3), 10q11.23-10q21.2, 15q22.2-15q23, and 16p12.2-16p12.1. Network analyses showed significant enrichment (false discovery rate <1 × 10(-5)) in genes that encode members of the JAK-STAT, cytokine, and chemokine signaling pathways, as well those involved in pathogenesis of measles. CONCLUSIONS: In a genetic analysis of 3308 AA IBD cases and controls, we found that many variants associated with IBD in Caucasians also showed association evidence with these diseases in AAs; we also found evidence for variants and loci not previously associated with IBD. The complex genetic factors that determine risk for or protection against IBD in different populations require further study.

6 Article A novel approach to detect cumulative genetic effects and genetic interactions in Crohn's disease. 2013

Wang, Ming-Hsi / Fiocchi, Claudio / Ripke, Stephan / Zhu, Xiaofeng / Duerr, Richard H / Achkar, Jean-Paul. ·Department of Gastroenterology and Hepatology, Digestive Disease Institute, Cleveland Clinic, Cleveland, Ohio 44195, USA. ·Inflamm Bowel Dis · Pubmed #23598818.

ABSTRACT: BACKGROUND: Genome-wide association studies have identified at least 71 Crohn's disease (CD) genetic risk loci, but the role of gene-gene interactions is unclear. The value of genetic variants in clinical practice is not defined because of limited explained heritability. METHODS: We examined model predictability of combining the 71 CD risk alleles and genetic interactions in an ongoing inflammatory bowel disease genome-wide association study. The Wellcome Trust Case Control Consortium inflammatory bowel disease genome-wide association study was used as a replicate cohort. We used logic regression, an adaptive regression methodology, to search for high-order binary predictors (e.g., single-nucleotide polymorphism [SNP] interactions). RESULTS: The combined 71 CD SNPs had good CD risk predictability (area under the curve of 0.75 and 0.73 in the 2 cohorts). Higher cumulative allele score predicted higher CD risk, but a relatively small difference in cumulative allele scores was observed between CD and controls (49 versus 47, P < 0.001). Through LR, we identified high-order genetic interactions and significantly improved the model predictability (area under the curve, from 0.75 to 0.77, P < 0.0001). A genetic interaction model, including NOD2, ATG16L1, IL10/IL19, C13orf31, and chr21q loci, was discovered and successfully replicated in the independent Wellcome Trust Case Control Consortium cohort. The explained heritability of the 71 CD SNPs alone was 24% and increased to 27% after adding the genetic interactions. CONCLUSIONS: A novel approach allowed the identification and replication of genetic interactions among NOD2, ATG16L1, IL10/IL19, C13orf31, and chr21q loci. CD risk can be predicted by a model of 71 CD loci and improved by adding genetic interactions.

7 Article Contribution of higher risk genes and European admixture to Crohn's disease in African Americans. 2012

Wang, Ming-Hsi / Okazaki, Toshihiko / Kugathasan, Subra / Cho, Judy H / Isaacs, Kim L / Lewis, James D / Smoot, Duane T / Valentine, John F / Kader, Howard A / Ford, Jean G / Harris, Mary L / Oliva-Hemker, Maria / Cuffari, Carmen / Torbenson, Michael S / Duerr, Richard H / Silverberg, Mark S / Rioux, John D / Taylor, Kent D / Nguyen, Geoffrey C / Wu, Yuqiong / Datta, Lisa W / Hooker, Stanley / Dassopoulos, Themistocles / Kittles, Rick A / Kao, Linda W H / Brant, Steven R. ·Lyn P. and Harvey M. Meyerhoff Inflammatory Bowel Disease Center, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. ·Inflamm Bowel Dis · Pubmed #22411504.

ABSTRACT: BACKGROUND: African Americans (AAs) are an admixed population of West African (WA) and European ancestry (EA). Crohn's disease (CD) susceptibility genes have not been established. We therefore evaluated the contribution of European admixture and major established risk genes to AA CD. METHODS: Ninety-seven admixture informative markers were genotyped for ancestry estimates using STRUCTURE. Overall, 354 AA CD cases and 354 ethnicity-matched controls were genotyped for total 21 single nucleotide polymorphisms (SNPs) in ATG16L1, NOD2, IBD5, IL23R and IRGM by TaqMan or direct sequencing. Association was evaluated by logistic regression, adjusted for ancestry. RESULTS: Mean EA was similar among the CD cases and controls (20.9% and 20.4%, respectively, P = 0.58). No significant admixture differences were observed among 211 to 227 cases stratified by phenotypic subclassifications including onset, surgery, site, and behavior. CD was associated with NOD2 carrier (6.93% CD, 2.15% Controls, P = 0.007), ATG16L1 Thr300Ala (36.1% CD, 29.3% Controls, P = 0.003), SLC22A4 and SLC22A5 (IBD5 locus) functional SNPs (Leu503Phe [10.5% CD, 7.6% Controls, P = 0.05] and g-207c [41.3% CD, 35.7% Controls, P = 0.03], respectively), and IL23R rs2201841 (18.2% CD, 13.8% Controls, P = 0.03), but not IRGM variants, nor three African ancestral NOD2 nonsynonymous variants. IBD5 risk was recessive. An all-minor allele IBD5 haplotype from EA was associated (P = 0.05), whereas a more common haplotype isolating g-207c was not. CONCLUSIONS: Specific functional gene variations contribute significantly to AA CD risk. Established NOD2, SLC22A4-A5, and ATG16L1 variants show increased CD risk, with IBD5 recessive. Although CD is more common in whites, European admixture is similar among AA cases and controls.