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  1. Article ; Online: Molecular Underpinnings of Severe Coronavirus Disease 2019.

    Plenge, Robert M

    JAMA

    2020  Volume 324, Issue 7, Page(s) 638–639

    MeSH term(s) COVID-19 ; Female ; Humans ; Pregnancy ; Pregnancy Complications, Infectious ; Pregnancy Outcome ; SARS-CoV-2
    Keywords covid19
    Language English
    Publishing date 2020-07-24
    Publishing country United States
    Document type Editorial ; Comment
    ZDB-ID 2958-0
    ISSN 1538-3598 ; 0254-9077 ; 0002-9955 ; 0098-7484
    ISSN (online) 1538-3598
    ISSN 0254-9077 ; 0002-9955 ; 0098-7484
    DOI 10.1001/jama.2020.14015
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  2. Article ; Online: Priority index for human genetics and drug discovery.

    Plenge, Robert M

    Nature genetics

    2019  Volume 51, Issue 7, Page(s) 1073–1075

    MeSH term(s) Drug Discovery ; Human Genetics ; Humans ; Phenotype
    Language English
    Publishing date 2019-06-28
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 1108734-1
    ISSN 1546-1718 ; 1061-4036
    ISSN (online) 1546-1718
    ISSN 1061-4036
    DOI 10.1038/s41588-019-0460-5
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  4. Article ; Online: Biomedicine: Human genes lost and their functions found.

    Plenge, Robert M

    Nature

    2017  Volume 544, Issue 7649, Page(s) 171–172

    Language English
    Publishing date 2017--12
    Publishing country England
    Document type Journal Article
    ZDB-ID 120714-3
    ISSN 1476-4687 ; 0028-0836
    ISSN (online) 1476-4687
    ISSN 0028-0836
    DOI 10.1038/544171a
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  5. Article ; Online: Disciplined approach to drug discovery and early development.

    Plenge, Robert M

    Science translational medicine

    2016  Volume 8, Issue 349, Page(s) 349ps15

    Abstract: Our modern health care system demands therapeutic interventions that improve the lives of patients. Unfortunately, decreased productivity in therapeutics research and development (R&D) has driven drug costs up while delivering insufficient value to ... ...

    Abstract Our modern health care system demands therapeutic interventions that improve the lives of patients. Unfortunately, decreased productivity in therapeutics research and development (R&D) has driven drug costs up while delivering insufficient value to patients. Here, I discuss a model of translational medicine that connects four components of the early R&D pipeline-causal human biology, therapeutic modality, biomarkers of target modulation, and proof-of-concept clinical trials. Whereas the individual components of this model are not new, technological advances and a disciplined approach to integrating all four areas offer hope for improving R&D productivity.
    Language English
    Publishing date 2016-07-27
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2518854-9
    ISSN 1946-6242 ; 1946-6234
    ISSN (online) 1946-6242
    ISSN 1946-6234
    DOI 10.1126/scitranslmed.aaf2608
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  6. Article ; Online: Unlocking the pathogenesis of celiac disease.

    Plenge, Robert M

    Nature genetics

    2010  Volume 42, Issue 4, Page(s) 281–282

    Abstract: A genome-wide association study reports more than a dozen new susceptibility loci for celiac disease. Analysis of eQTL data from these and previously established risk loci sheds light on the genetic pathways underlying this common autoimmune disease. ...

    Abstract A genome-wide association study reports more than a dozen new susceptibility loci for celiac disease. Analysis of eQTL data from these and previously established risk loci sheds light on the genetic pathways underlying this common autoimmune disease.
    MeSH term(s) Celiac Disease/genetics ; Celiac Disease/immunology ; Genetic Predisposition to Disease ; Genome-Wide Association Study ; Humans ; Polymorphism, Single Nucleotide ; Risk Factors
    Language English
    Publishing date 2010-03-28
    Publishing country United States
    Document type Comment ; News
    ZDB-ID 1108734-1
    ISSN 1546-1718 ; 1061-4036
    ISSN (online) 1546-1718
    ISSN 1061-4036
    DOI 10.1038/ng0410-281
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  7. Article ; Online: Rare protection against type 1 diabetes.

    Plenge, Robert M

    Genome biology

    2009  Volume 10, Issue 5, Page(s) 219

    Abstract: A large population study using ultra-high-throughput DNA sequencing to re-sequence a genetic locus associated with type 1 diabetes reveals rare protective alleles. ...

    Abstract A large population study using ultra-high-throughput DNA sequencing to re-sequence a genetic locus associated with type 1 diabetes reveals rare protective alleles.
    MeSH term(s) DEAD-box RNA Helicases/genetics ; Diabetes Mellitus, Type 1/genetics ; Genetic Predisposition to Disease ; Humans ; Interferon-Induced Helicase, IFIH1 ; Polymorphism, Single Nucleotide ; Sequence Analysis, DNA
    Chemical Substances IFIH1 protein, human (EC 3.6.1.-) ; DEAD-box RNA Helicases (EC 3.6.4.13) ; Interferon-Induced Helicase, IFIH1 (EC 3.6.4.13)
    Language English
    Publishing date 2009-05-15
    Publishing country England
    Document type Journal Article
    ZDB-ID 2040529-7
    ISSN 1474-760X ; 1474-760X
    ISSN (online) 1474-760X
    ISSN 1474-760X
    DOI 10.1186/gb-2009-10-5-219
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  8. Article ; Online: Rheumatoid arthritis genetics: 2009 update.

    Plenge, Robert M

    Current rheumatology reports

    2009  Volume 11, Issue 5, Page(s) 351–356

    Abstract: Recent human genetic discoveries have increased our understanding of rheumatoid arthritis (RA) susceptibility. Genome-wide association studies have expanded the number of validated RA risk loci beyond HLA-DRB1 "shared epitope" alleles to include ... ...

    Abstract Recent human genetic discoveries have increased our understanding of rheumatoid arthritis (RA) susceptibility. Genome-wide association studies have expanded the number of validated RA risk loci beyond HLA-DRB1 "shared epitope" alleles to include additional major histocompatibility complex (MHC) risk alleles and more than 10 regions outside the MHC. The newly discovered risk alleles are common in the general population, have a modest effect on RA risk, and together explain less than 5% of the variance in disease risk. Whereas the actual causal mutation and causal gene for most loci remain to be determined, these studies are beginning to reveal general themes: many risk loci are associated with other autoimmune diseases; many genes fall within discrete biological pathways (eg, the nuclear factor kappa-light-chain-enhancer of activated B cells signaling pathway); and human genetics can group diseases into clinically meaningful subset categories (eg, presence or absence of autoantibodies). This review discusses recent RA genetic discoveries in terms of their potential to improve patient care.
    MeSH term(s) Arthritis, Rheumatoid/genetics ; Arthritis, Rheumatoid/therapy ; Genetic Predisposition to Disease ; Genome-Wide Association Study ; Humans ; Immunogenetics ; Major Histocompatibility Complex/genetics ; Precision Medicine
    Language English
    Publishing date 2009-09-23
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2057357-1
    ISSN 1534-6307 ; 1523-3774
    ISSN (online) 1534-6307
    ISSN 1523-3774
    DOI 10.1007/s11926-009-0050-0
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  9. Article ; Online: Recent progress in rheumatoid arthritis genetics: one step towards improved patient care.

    Plenge, Robert M

    Current opinion in rheumatology

    2009  Volume 21, Issue 3, Page(s) 262–271

    Abstract: Purpose of review: Recent human genetic discoveries have increased our understanding of rheumatoid arthritis (RA) susceptibility. These discoveries are reviewed and placed in the context of potential important clinical applications.: Recent findings: ...

    Abstract Purpose of review: Recent human genetic discoveries have increased our understanding of rheumatoid arthritis (RA) susceptibility. These discoveries are reviewed and placed in the context of potential important clinical applications.
    Recent findings: Genome-wide association studies and related methodologies have expanded the number of validated RA risk loci beyond HLA-DRB1 'shared epitope' alleles to include additional major histocompatibility complex risk alleles and more than 10 regions outside the major histocompatibility complex locus. The newly discovered risk alleles are common in the general population, and most have a modest effect on risk of RA (odds ratio approximately 1.15 per copy of each risk allele). Although the actual causal mutation and causal gene for most loci remain to be determined, these studies are beginning to reveal general themes: many risk loci are associated with other autoimmune diseases, many genes fall within discrete biological pathways (e.g., the NF-kappaB signaling pathway), and human genetics can subset disease into clinically meaningful categories (e.g., presence or absence of autoantibodies).
    Summary: Approximately one-third of the genetic basis of RA can be explained by known risk loci. Future studies need to pinpoint the actual causal mutations, expand the number of risk loci, and translate these discoveries to improve care of patients with RA.
    MeSH term(s) Alleles ; Arthritis, Rheumatoid/genetics ; Arthritis, Rheumatoid/immunology ; Arthritis, Rheumatoid/therapy ; Autoimmunity/genetics ; CD40 Antigens/genetics ; Ethnic Groups/genetics ; Gene Dosage ; Genetic Predisposition to Disease ; Genetic Variation ; Genome-Wide Association Study ; HLA-DR Antigens/genetics ; HLA-DRB1 Chains ; Humans ; Immunogenetics ; Models, Genetic ; NF-kappa B/genetics ; Peptides, Cyclic/genetics ; Risk Factors
    Chemical Substances CD40 Antigens ; HLA-DR Antigens ; HLA-DRB1 Chains ; NF-kappa B ; Peptides, Cyclic ; cyclic citrullinated peptide
    Language English
    Publishing date 2009-05
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1045317-9
    ISSN 1531-6963 ; 1040-8711
    ISSN (online) 1531-6963
    ISSN 1040-8711
    DOI 10.1097/BOR.0b013e32832a2e2d
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  10. Article ; Online: Shared genetic risk factors for type 1 diabetes and celiac disease.

    Plenge, Robert M

    The New England journal of medicine

    2008  Volume 359, Issue 26, Page(s) 2837–2838

    MeSH term(s) Autoimmunity/genetics ; Celiac Disease/genetics ; Diabetes Mellitus, Type 1/genetics ; Genetic Predisposition to Disease ; Humans ; Risk Factors
    Language English
    Publishing date 2008-12-25
    Publishing country United States
    Document type Comment ; Editorial
    ZDB-ID 207154-x
    ISSN 1533-4406 ; 0028-4793
    ISSN (online) 1533-4406
    ISSN 0028-4793
    DOI 10.1056/NEJMe0809719
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