Abstract: Provided herein are methods of treating B7-H1-expressing tumors comprising administering an effective amount of MEDI4736 or an antigen-binding fragment thereof.

Abstract: Provided herein are methods of treating B7-H1-expressing tumors comprising administering an effective amount of MEDI4736 or an antigen-binding fragment thereof.

Abstract: The present invention relates to the use of components of the IL23 pathway as biomarkers, e.g., IL22, LCN2 and combinations thereof, to stratify or identify populations of patients suffering from IL23-mediated diseases (e.g., Crohn's disease) responsive to treatment with an anti-IL23 antagonist (including, e.g., anti-IL23 antibodies or antigen-binding fragments thereof). Levels of IL23 pathway biomarkers above or below a predetermined threshold can be used, for example, (i) to determine whether a patient with an IL23-mediated disease or disorder such a Crohn's disease is eligible or non-eligible for treatment with a therapeutic agent (e.g., an anti-IL23 antibody), (ii) to determine whether treatment with a certain agent should be commenced, suspended, or modified, (iii) to diagnose whether the IL23-mediated disease is treatable or not treatable with a specific therapeutic agent, or (iv) to predict the outcome of treating the IL23-mediated disease with a specific therapeutic agent.

Abstract: The present invention relates to the use of the Chemokine (C—C motif) ligand 20 (CCL20) as a biomarker to stratify or identify populations of patients suffering from interleukin-23 (IL23)-mediated diseases (e.g., Crohn's disease) responsive to treatment with an, anti-IL23 antagonist (including, e.g., anti-IL23 antibodies). Levels of CCL20 above or below a predetermined threshold can be used, for example, (i) to determine whether a patient with an IL23-mediated disease or disorder such a Crohn's disease is eligible or non-eligible for treatment with a therapeutic agent, (ii) to determine whether treatment with a certain agent should be commenced, suspended, or modified, (iii) to diagnose whether the IL23-mediated disease is treatable or not treatable with a specific therapeutic agent, or (iv) to predict the outcome of treating the IL23-mediated disease with a specific therapeutic agent. CCL20 can be used in combination with other IL23 pathway biomarkers such as IL22 and/or lipocalin-2 (LCN2).

Abstract: The present invention relates to the use of the Chemokine (C—C motif) ligand 20 (CCL20) as a biomarker to stratify or identify populations of patients suffering from interleukin-23 (IL23)-mediated diseases (e.g., Crohn's disease) responsive to treatment with an, anti-IL23 antagonist (including, e.g., anti-IL23 antibodies). Levels of CCL20 above or below a predetermined threshold can be used, for example, (i) to determine whether a patient with an IL23-mediated disease or disorder such a Crohn's disease is eligible or non-eligible for treatment with a therapeutic agent, (ii) to determine whether treatment with a certain agent should be commenced, suspended, or modified, (iii) to diagnose whether the IL23-mediated disease is treatable or not treatable with a specific therapeutic agent, or (iv) to predict the outcome of treating the IL23-mediated disease with a specific therapeutic agent. CCL20 can be used in combination with other IL23 pathway biomarkers such as IL22 and/or lipocalin-2 (LCN2).

Abstract: The present invention relates to the use of components of the IL23 pathway as biomarkers, e.g., IL22, LCN2 and combinations thereof, to stratify or identify populations of patients suffering from IL23-mediated diseases (e.g., Crohn's disease) responsive to treatment with an anti-IL23 antagonist (including, e.g., anti-IL23 antibodies or antigen-binding fragments thereof). Levels of IL23 pathway biomarkers above or below a predetermined threshold can be used, for example, (i) to determine whether a patient with an IL23-mediated disease or disorder such a Crohn's disease is eligible or non-eligible for treatment with a therapeutic agent (e.g., an ant-IL23 antibody), (ii) to determine whether treatment with a certain agent should be commenced, suspended, or modified, (iii) to diagnose whether the IL23-mediated disease is treatable or not treatable with a specific therapeutic agent, or (iv) to predict the outcome of treating the IL23-mediated disease with a specific therapeutic agent.

Abstract: Provided herein are methods of treating B7-H1-expressing tumors comprising administering an effective amount of MEDI4736 or an antigen-binding fragment thereof.

Abstract: The present invention relates to the use of the Chemokine (C—C motif) ligand 20 (CCL20) as a biomarker to stratify or identify populations of patients suffering from interleukin-23 (IL23)-mediated diseases (e.g., Crohn's disease) responsive to treatment with an, anti-IL23 antagonist (including, e.g., anti-IL23 antibodies). Levels of CCL20 above or below a predetermined threshold can be used, for example, (i) to determine whether a patient with an IL23-mediated disease or disorder such a Crohn's disease is eligible or non-eligible for treatment with a therapeutic agent, (ii) to determine whether treatment with a certain agent should be commenced, suspended, or modified, (iii) to diagnose whether the IL23-mediated disease is treatable or not treatable with a specific therapeutic agent, or (iv) to predict the outcome of treating the IL23-mediated disease with a specific therapeutic agent. CCL20 can be used in combination with other IL23 pathway biomarkers such as IL22 and/or lipocalin-2 (LCN2).

Abstract: Provided herein are methods of treating B7-H1-expressing tumors comprising administering an effective amount of MEDI4736 or an antigen-binding fragment thereof.

Abstract: Provided herein are methods of treating B7-H1-expressing tumors comprising administering an effective amount of MEDI4736 or an antigen-binding fragment thereof.

Abstract: Disclosed are methods for treating cancer (e.g., solid tumor cancers, lung cancer, bladder head and neck cancer) with an anti-PD-L1 antibody in a patient identified as being responsive to anti-PD-L1 antibody therapy by detecting a mutation in one or more disclosed circulating tumor DNA (ctDNA) markers. Also disclosed are methods for determining the efficacy of anti-PD-L1 therapeutic antibody treatment in a patient having lung cancer or bladder cancer comprising detecting variant allele frequency in ctDNA in plasma samples and determining the difference of the variant allele frequency in ctDNA between the first and at least second plasma samples, wherein a decrease in the variant allele frequency in the at least second plasma sample relative to the first plasma sample identifies the anti-PD-L1 antibody treatment as effective.

Abstract: The present invention relates to the use of components of the IL23 pathway as biomarkers, e.g., IL22, LCN2 and combinations thereof, to stratify or identify populations of patients suffering from IL23-mediated diseases (e.g., Crohn's disease) responsive to treatment with an anti-IL23 antagonist (including, e.g., anti-IL23 antibodies or antigen-binding fragments thereof). Levels of IL23 pathway biomarkers above or below a predetermined threshold can be used, for example, (i) to determine whether a patient with an IL23-mediated disease or disorder such a Crohn's disease is eligible or non-eligible for treatment with a therapeutic agent (e.g., an ant-IL23 antibody), (ii) to determine whether treatment with a certain agent should be commenced, suspended, or modified, (iii) to diagnose whether the IL23-mediated disease is treatable or not treatable with a specific therapeutic agent, or (iv) to predict the outcome of treating the IL23-mediated disease with a specific therapeutic agent.

Abstract: The disclosure provides methods for treating a subject having a type I IFN-mediated disease or disorder comprising administration of a fixed does of an anti-interferon alpha receptor antibody. The disclosure also provides methods for suppressing a type I interferon (IFN) gene signature (GS) in a subject. In addition, the disclosure provides methods of prognosing or monitoring disease progression in a subject having a type I IFN-mediated disease or disorder, methods of predicting a dosage regimen, methods of identifying a candidate therapeutic agent, methods of identifying a patient as a candidate for a therapeutic agent, and methods of designating a personalized therapy.

Abstract: Provided herein are methods of treating B7-H1-expressing tumors comprising administering an effective amount of MEDI4736 or an antigen-binding fragment thereof.

Abstract: The present disclosure encompasses type-I IFN and IFN?-induced PD marker expression profiles, kits, and methods for identifying such IFN?-induced PD marker expression profiles. The type-I IFN and IFN?-induced PD marker expression profiles may also be used in, for example, methods of treating patients having a type-I IFN or IFN?-mediated disorder, methods of monitoring disease progression of patients receiving treatment with a therapeutic agent that modulates type 1 interferon activity, identifying patients as candidates to receive a therapeutic that binds to and neutralizes IFN? activity, and in diagnosing or providing a prognosis to patients having IFN?-induced disorders.

Abstract: The disclosure provides methods for treating a subject having a type I IFN-mediated disease or disorder comprising administration of a fixed does of an anti-interferon alpha receptor antibody. The disclosure also provides methods for suppressing a type I interferon (IFN) gene signature (GS) in a subject. In addition, the disclosure provides methods of prognosing or monitoring disease progression in a subject having a type I IFN-mediated disease or disorder, methods of predicting a dosage regimen, methods of identifying a candidate therapeutic agent, methods of identifying a patient as a candidate for a therapeutic agent, and methods of designating a personalized therapy.

Abstract: The present disclosure encompasses type-I IFN and IFN?-induced PD marker expression profiles, kits, and methods for identifying such IFN?-induced PD marker expression profiles. The type-I IFN and IFN?-induced PD marker expression profiles may also be used in, for example, methods of treating patients having a type-I IFN or IFN?-mediated disorder, methods of monitoring disease progression of patients receiving treatment with a therapeutic agent that modulates type 1 interferon activity, identifying patients as candidates to receive a therapeutic that binds to and neutralizes IFN? activity, and in diagnosing or providing a prognosis to patients having IFN?-induced disorders.

Abstract: The present invention encompasses miRNA profiles and type-I IFN/IFN?-induced PD marker profiles in inflammatory or autoimmune disorders, such as myositis. The profiles may also be used in, for example, methods of treating patients, methods of monitoring disease progression of patients, and in diagnosing or providing a prognosis to patients having inflammatory or autoimmune disorders.

Abstract: The present invention includes methods of predicting hepatotoxicity of test agents and methods of generating hepatotoxicity prediction models using algorithms for analyzing quantitative gene expression information. The invention also includes microarrays, computer systems comprising the toxicity prediction models, as well as methods of using the computer systems by remote users for determining the toxicity of test agents.

Abstract: The present invention is based on the elucidation of the global changes in gene expression and the identification of toxicity markers in tissues or cells exposed to a known toxin. The genes may be used as toxicity markers in drug screening and toxicity assays. The invention includes a database of genes characterized by toxin-induced differential expression that is designed for use with microarrays and other solid-phase probes.