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Keywords {🔍}

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Topics {✒️}

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Questions {❓}

• What underlying biological basis could explain why blockade of the IL-6 pathway causes robust clinical responses in a different patient population to that responding to anti-TNFα blockade?

Schema {🗺️}

WebPage:
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         headline:Synovial phenotypes in rheumatoid arthritis correlate with response to biologic therapeutics
         description:Rheumatoid arthritis (RA) is a complex and clinically heterogeneous autoimmune disease. Currently, the relationship between pathogenic molecular drivers of disease in RA and therapeutic response is poorly understood. We analyzed synovial tissue samples from two RA cohorts of 49 and 20 patients using a combination of global gene expression, histologic and cellular analyses, and analysis of gene expression data from two further publicly available RA cohorts. To identify candidate serum biomarkers that correspond to differential synovial biology and clinical response to targeted therapies, we performed pre-treatment biomarker analysis compared with therapeutic outcome at week 24 in serum samples from 198 patients from the ADACTA (ADalimumab ACTemrA) phase 4 trial of tocilizumab (anti-IL-6R) monotherapy versus adalimumab (anti-TNFα) monotherapy. We documented evidence for four major phenotypes of RA synovium – lymphoid, myeloid, low inflammatory, and fibroid - each with distinct underlying gene expression signatures. We observed that baseline synovial myeloid, but not lymphoid, gene signature expression was higher in patients with good compared with poor European league against rheumatism (EULAR) clinical response to anti-TNFα therapy at week 16 (P =0.011). We observed that high baseline serum soluble intercellular adhesion molecule 1 (sICAM1), associated with the myeloid phenotype, and high serum C-X-C motif chemokine 13 (CXCL13), associated with the lymphoid phenotype, had differential relationships with clinical response to anti-TNFα compared with anti-IL6R treatment. sICAM1-high/CXCL13-low patients showed the highest week 24 American College of Rheumatology (ACR) 50 response rate to anti-TNFα treatment as compared with sICAM1-low/CXCL13-high patients (42% versus 13%, respectively, P =0.05) while anti-IL-6R patients showed the opposite relationship with these biomarker subgroups (ACR50 20% versus 69%, P =0.004). These data demonstrate that underlying molecular and cellular heterogeneity in RA impacts clinical outcome to therapies targeting different biological pathways, with patients with the myeloid phenotype exhibiting the most robust response to anti-TNFα. These data suggest a path to identify and validate serum biomarkers that predict response to targeted therapies in rheumatoid arthritis and possibly other autoimmune diseases. ClinicalTrials.gov NCT01119859
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            Orthopedics
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      headline:Synovial phenotypes in rheumatoid arthritis correlate with response to biologic therapeutics
      description:Rheumatoid arthritis (RA) is a complex and clinically heterogeneous autoimmune disease. Currently, the relationship between pathogenic molecular drivers of disease in RA and therapeutic response is poorly understood. We analyzed synovial tissue samples from two RA cohorts of 49 and 20 patients using a combination of global gene expression, histologic and cellular analyses, and analysis of gene expression data from two further publicly available RA cohorts. To identify candidate serum biomarkers that correspond to differential synovial biology and clinical response to targeted therapies, we performed pre-treatment biomarker analysis compared with therapeutic outcome at week 24 in serum samples from 198 patients from the ADACTA (ADalimumab ACTemrA) phase 4 trial of tocilizumab (anti-IL-6R) monotherapy versus adalimumab (anti-TNFα) monotherapy. We documented evidence for four major phenotypes of RA synovium – lymphoid, myeloid, low inflammatory, and fibroid - each with distinct underlying gene expression signatures. We observed that baseline synovial myeloid, but not lymphoid, gene signature expression was higher in patients with good compared with poor European league against rheumatism (EULAR) clinical response to anti-TNFα therapy at week 16 (P =0.011). We observed that high baseline serum soluble intercellular adhesion molecule 1 (sICAM1), associated with the myeloid phenotype, and high serum C-X-C motif chemokine 13 (CXCL13), associated with the lymphoid phenotype, had differential relationships with clinical response to anti-TNFα compared with anti-IL6R treatment. sICAM1-high/CXCL13-low patients showed the highest week 24 American College of Rheumatology (ACR) 50 response rate to anti-TNFα treatment as compared with sICAM1-low/CXCL13-high patients (42% versus 13%, respectively, P =0.05) while anti-IL-6R patients showed the opposite relationship with these biomarker subgroups (ACR50 20% versus 69%, P =0.004). These data demonstrate that underlying molecular and cellular heterogeneity in RA impacts clinical outcome to therapies targeting different biological pathways, with patients with the myeloid phenotype exhibiting the most robust response to anti-TNFα. These data suggest a path to identify and validate serum biomarkers that predict response to targeted therapies in rheumatoid arthritis and possibly other autoimmune diseases. ClinicalTrials.gov NCT01119859
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      dateModified:2014-04-30T00:00:00Z
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      pageEnd:18
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         Adalimumab
         Synovial Tissue
         Tocilizumab
         Rheumatoid Arthritis Synovium
         ACR50 Response
         Rheumatology
         Orthopedics
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            name:Genentech
            address:
               name:Departments of Immunology Discovery, Genentech, South San Francisco, USA
               type:PostalAddress
            type:Organization
      name:Cécile TJ Holweg
      affiliation:
            name:Genentech
            address:
               name:ITGR Diagnostics Discovery, Genentech, South San Francisco, USA
               type:PostalAddress
            type:Organization
      name:Sarah K Kummerfeld
      affiliation:
            name:Genentech
            address:
               name:Bioinformatics and Computational Biology, Genentech, South San Francisco, USA
               type:PostalAddress
            type:Organization
      name:David F Choy
      affiliation:
            name:Genentech
            address:
               name:ITGR Diagnostics Discovery, Genentech, South San Francisco, USA
               type:PostalAddress
            type:Organization
      name:A Francesca Setiadi
      affiliation:
            name:Genentech
            address:
               name:ITGR Diagnostics Discovery, Genentech, South San Francisco, USA
               type:PostalAddress
            type:Organization
      name:Jason A Hackney
      affiliation:
            name:Genentech
            address:
               name:Bioinformatics and Computational Biology, Genentech, South San Francisco, USA
               type:PostalAddress
            type:Organization
      name:Peter M Haverty
      affiliation:
            name:Genentech
            address:
               name:Bioinformatics and Computational Biology, Genentech, South San Francisco, USA
               type:PostalAddress
            type:Organization
      name:Houston Gilbert
      affiliation:
            name:Genentech
            address:
               name:Non-clinical Biostatistics, Genentech, South San Francisco, USA
               type:PostalAddress
            type:Organization
      name:Wei Yu Lin
      affiliation:
            name:Genentech
            address:
               name:Departments of Immunology Discovery, Genentech, South San Francisco, USA
               type:PostalAddress
            type:Organization
      name:Lauri Diehl
      affiliation:
            name:Genentech
            address:
               name:Pathology, Genentech, South San Francisco, USA
               type:PostalAddress
            type:Organization
      name:S Fischer
      affiliation:
            name:Genentech
            address:
               name:Bioanalytical Sciences, Genentech, South San Francisco, USA
               type:PostalAddress
            type:Organization
      name:An Song
      affiliation:
            name:Genentech
            address:
               name:Bioanalytical Sciences, Genentech, South San Francisco, USA
               type:PostalAddress
            type:Organization
      name:David Musselman
      affiliation:
            name:Genentech
            address:
               name:Product Development, Genentech, South San Francisco, USA
               type:PostalAddress
            type:Organization
      name:Micki Klearman
      affiliation:
            name:Genentech
            address:
               name:Product Development, Genentech, South San Francisco, USA
               type:PostalAddress
            type:Organization
      name:Cem Gabay
      affiliation:
            name:University Hospital of Geneva
            address:
               name:University Hospital of Geneva, Geneva, Switzerland
               type:PostalAddress
            type:Organization
      name:Arthur Kavanaugh
      affiliation:
            name:University of California San Diego
            address:
               name:University of California San Diego, San Diego, USA
               type:PostalAddress
            type:Organization
      name:Judith Endres
      affiliation:
            name:University of Michigan Medical School
            address:
               name:Rheumatic Disease Core Center and Division of Rheumatology, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, USA
               type:PostalAddress
            type:Organization
      name:David A Fox
      affiliation:
            name:University of Michigan Medical School
            address:
               name:Rheumatic Disease Core Center and Division of Rheumatology, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, USA
               type:PostalAddress
            type:Organization
      name:Flavius Martin
      affiliation:
            name:Genentech
            address:
               name:Departments of Immunology Discovery, Genentech, South San Francisco, USA
               type:PostalAddress
            type:Organization
            name:Inflammation Therapeutic Area, Amgen
            address:
               name:Inflammation Therapeutic Area, Amgen, Seattle, USA
               type:PostalAddress
            type:Organization
      name:Michael J Townsend
      affiliation:
            name:Genentech
            address:
               name:ITGR Diagnostics Discovery, Genentech, South San Francisco, USA
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Departments of Immunology Discovery, Genentech, South San Francisco, USA
      name:ITGR Diagnostics Discovery, Genentech, South San Francisco, USA
      name:Bioinformatics and Computational Biology, Genentech, South San Francisco, USA
      name:ITGR Diagnostics Discovery, Genentech, South San Francisco, USA
      name:ITGR Diagnostics Discovery, Genentech, South San Francisco, USA
      name:Bioinformatics and Computational Biology, Genentech, South San Francisco, USA
      name:Bioinformatics and Computational Biology, Genentech, South San Francisco, USA
      name:Non-clinical Biostatistics, Genentech, South San Francisco, USA
      name:Departments of Immunology Discovery, Genentech, South San Francisco, USA
      name:Pathology, Genentech, South San Francisco, USA
      name:Bioanalytical Sciences, Genentech, South San Francisco, USA
      name:Bioanalytical Sciences, Genentech, South San Francisco, USA
      name:Product Development, Genentech, South San Francisco, USA
      name:Product Development, Genentech, South San Francisco, USA
      name:University Hospital of Geneva, Geneva, Switzerland
      name:University of California San Diego, San Diego, USA
      name:Rheumatic Disease Core Center and Division of Rheumatology, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, USA
      name:Rheumatic Disease Core Center and Division of Rheumatology, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, USA
      name:Departments of Immunology Discovery, Genentech, South San Francisco, USA
      name:Inflammation Therapeutic Area, Amgen, Seattle, USA
      name:ITGR Diagnostics Discovery, Genentech, South San Francisco, USA

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