The present invention provides a pharmaceutical composition for the treatment of patients having ovarian cancer, lung cancer or mesothelioma and showing a Selection Factor of −30% or below, comprising a therapeutically effective amount of ipilimumab, and optionally a pharmaceutically acceptable diluent or carrier, wherein the patient is selected on the basis of a positive response to an ex vivo three-dimensional (3D) patient derived tumour culture, the method comprising: (a) preparing a three-dimensional, optionally size-normalised, tumour culture from a patient-derived tumour sample in a multitude of replicates; (b) adding one or more immunotherapeutic agents to the culture, and (c) culturing for a pre-defined time period; and (d) determining the effect that the one or more immunotherapeutic agents has on the tumour cell aggregates by measuring the total area of objects in the culture that are above a threshold area associated with tumour cell aggregates, and the total area of objects that are below a threshold associated with immune cells, using three-dimensional imaging of the cell culture; wherein if following culturing with a composition comprising ipilimumab, the total area of the large objects decreases and/or the total area of the small objects increases relative to a control the patient is treated with ipilimumab.

Methods of altering viral latency, sensitizing EBV+ tumors, or modulating viral immunogenicity, are provided.

The present invention is primarily directed to provide a new process capable of performing direct conversion of or induction from a somatic cell to brown adipocytes with low molecular weight compounds, without performing artificial gene transfer.

The present invention includes, for example, a process for producing brown adipocytes by direct differentiation induction from somatic cells, comprising a step of culturing a somatic cell in a serum-free differentiation induction medium in the presence of a selective PPARγ agonist and a cAMP inducer.

According to the present invention, direct conversion of or induction from somatic cells to brown adipocytes can be effectively performed without gene transfer. The brown adipocytes obtained by the present invention are useful as regenerative medicine, models of human brown adipocytes and human beige cells, and the like.

The disclosure relates to a plurality of cells, compositions and methods for identifying modulators of a target protein. The cells, compositions and methods comprise a (i) a target domain gene (ii) an intracellular chimeric G-protein alpha subunit comprising an endogenous G-protein alpha subunit with a humanized C-terminus; and (iii) an inducible reporter, wherein the expression of the reporter is dependent on the activation of the target domain encoded by target domain gene, and wherein the target domain gene comprises a barcode. The disclosure further relates to a host cell comprising a plurality of exogenous landing pads integrated in the host cell's genome, wherein each exogenous landing pad is integrated at a safe harbor genome loci in the host cell's genome.

The present invention relates to methods for determining affinity, binding kinetics and/or concentration of an antibody or of an antibody mixture specific for a virus using virus-like particles (VLPs) and/or live viruses or inactivated viruses attached to biosensors. Further, the present invention relates to the VLPs and live or inactivated viruses attached to biosensors and methods for producing them.

The present disclosure provides antibodies that specifically bind to human glucocorticoid-induced TNFR family related receptor (GITR) and compositions comprising such antibodies. In a specific aspect, the antibodies specifically bind to human GITR and modulate GITR activity, e.g., enhance, activate or induce GITR activity, utilizing such antibodies. The present disclosure also provides methods for treating disorders, such as cancer and infectious diseases, by administering an antibody that specifically binds to human GITR and modulates GITR activity e.g., enhances, activates or induces GITR activity.

This invention relates to agents that are inhibitors or activators of variant forms of endogenous proteins and novel methods of identifying such variants. Of particular interest are inhibitors and activators of endogenous protein variants, encoded by genes which have mutated, which variants often arise or are at least first identified as having arisen following exposure to a chemical agent which is known to be an inhibitor or activator of the corresponding unmutated endogenous protein.

The present disclosure provides methods for processing extracellular vesicles in which the extracellular vesicles are not purified, prior to contacting with a fluorescent staining dye or an antibody. By utilizing a centrifugal filter, excess staining dye or antibody can be readily removed prior to analysis of one or more characteristics of the extracellular vesicles. The methods provide rapid and simple processing and analysis, while maintaining a high concentration of extracellular vesicles.

A micropeptide HMMW of a new structure and an application thereof, and relates to the field of biomedical research and development is prpvided. The micropeptide HMMW is obtained by encoding human lncRNA, and a recombinant vector is constructed so that objective cells perform high expression on the micropeptide HMMW, which can inhibit proliferation and migration of multiple solid tumors including the head and neck cancer, thyroid cancer, lung cancer, esophageal squamous cell carcinoma, stomach cancer, breast cancer, kidney cancer, skin cancer and the like, and growth of tumors in the body. The micropeptide HMMW has potential value for new drug development, important tumor detection and treatment value.

The present application provides detectable compounds useful for identifying compounds that bind (e.g., inhibit) MmpL3. Methods of identifying compounds that bind and/or inhibit MmpL3 are also provided.