The present invention relates to combination therapies useful for the treatment of cancer. In particular, the invention relates to a therapeutic combination which comprises a PD-1 antagonist, an ATR inhibitor and a platinating agent.

The present invention generally relates to pharmacokinetic and pharmacodynamics markers for cancer therapeutic regimens and methods of treating cancer. Oncolytic virus probes that comprise a nucleic acid encoding soluble interferon beta (IFNβ) and methods for use thereof are provided.

Disclosed herein are methods in which an individual with multiple sclerosis (MS) can be classified into one of six subject groups, each subject group predictive for the patient's responsiveness to an interferon-β (IFN-β) therapy. The individual with MS can be classified according to the individual's serum marker levels, e.g., at baseline or following treatment with therapy. Depending on the classification, the individual with MS can be treated with standard therapies (e.g. IFN-β) or one or more alternative therapies with or without IFN-β.

The present disclosure relates, in general, to methods for screening for modulators of IFNβ activity using a GLuc/SEAP dual reporter system.

The present invention provides a prophylactic agent, onset-suppressing agent, or therapeutic agent for progressive immune demyelinating diseases comprising, as an active ingredient, a substance capable of suppressing or inhibiting production of prolactin.

Provided are methods of modulating the type I interferon (IFN) pathway in an individual. The methods involve administering to an individual one or more agents that inhibit expression or function of METTL3, or METTL14, or ALKBH5, thereby modulating the type I IFN pathway. The agent that inhibits the expression and/or function ALKBH5 results in decreased interferon β cytokine production and/or decreased IFNB1 mRNA, and is useful for treating autoimmune and inflammatory conditions. The agent that inhibits expression or function of METTL3 and/or METTL14 result in increased IPNβ cytokine production and/or increased IFNB 1 mRNA, and is useful for treating infections and cancer. Methods for screening and identifying enzyme inhibitors are also provided.

The present invention provides a prophylactic agent, onset-suppressing agent, or therapeutic agent for progressive immune demyelinating diseases comprising, as an active ingredient, a substance capable of suppressing or inhibiting production of prolactin.

The present invention provides a cell-based method for identification of an adjuvant and adjuvant combinations and a composition of a vaccine that includes the adjuvant and adjuvant combinations. The method comprises the steps: using an adjuvant or adjuvant combination to treat at least one type of antigen-presenting cells and measuring amount of at least one cytokine produced by the antigen-presenting cells.

The present disclosure provides a method of measuring the production of a cytokine in a sample in response to an agonist to determine responsiveness of a patient to immunotherapy. The present disclosure also provides a method of treating a cancer patient with an oncolytic viral therapy when a sample from the patient has a certain level of anti-viral antibodies. Further, the present disclosure describes, in part, an immune competence blood test that allows for one skilled in the art to determine if a tumor is immunoproficient to respond to an immunotherapy.

The disclosure relates to methods and assay that assists in the diagnosis of autoimmune and chronic inflammatory disorders such as systemic lupus erythematosus and rheumatoid arthritis by analyzing drug-responsiveness of an interferon signal in a hematological sample (e.g., blood) obtained from a human subject. The assay involves comparing the interferon signal in a control aliquot of the sample with the same interferon sample in an aliquot that has been exposed to a therapeutic modality (e.g., combined with a drug) that is known to be efficacious to treat the disorder. A significant difference between the interferon signals of the control and treated aliquots that corresponds to a characteristic interferon signature for the disorder indicates that the subject is afflicted with, or is likely to develop, the disorder.