The present invention relates to a method for the diagnosis, prognosis, risk assessment, risk stratification, monitoring, therapy guidance and/or therapy control of cancer in a subject comprising the determination of the level of an anti-PD1 antibody and/or an anti-PD-L1 antibody in a sample of a bodily fluid of said subject.

The p21 biomarker is utilized in the evaluation of whether a patient is suffering from kidney injury or failure, and can be used in methods of treating kidney injury or failure by determining the appropriateness of one or more of initiating renal replacement therapy, withdrawing delivery of compounds that are known to be damaging to the kidney, delaying or avoiding procedures that are known to be damaging to the kidney, and modifying diuretic administration.

This disclosure describes the characteristics of the “energetic” cancer stem cell (e-CSC) phenotype. This distinct sub-population of cancer stem cells (CSCs) has a unique energetic profile compared to bulk CSCs, being more glycolytic, having higher mitochondrial mass and elevated oxidative metabolism. e-CSCs also show an increased capacity to undergo cell cycle progression, enhanced anchorage-independent growth, and ALDH-positivity. The e-CSC phenotype presents new targets for cancer therapeutics, and in particular the anti-oxidant response, mitochondrial energy production, and mitochondrial biogenesis of e-CSCs makes them highly susceptible to mitochondrial inhibitors that target e-CSC anti-oxidant response, mitochondrial energy production, and mitochondrial biogenesis. Gene products for e-CSCs are disclosed, as well as classes of mitochondrial inhibiting therapeutic agents. Also disclosed are methods for identifying and separating e-CSCs from bulk cell populations.

Provided are a novel determination method, diagnostic probe, and diagnostic kit for inflammatory bowel disease. A method for determining inflammatory bowel disease includes measuring an anti-endothelial cell protein C receptor antibody (anti-EPCR antibody) in a sample collected from a subject.

A prognostic method, and a kit, for determining the risk of relapse of renal cancer of the clear cell renal carcinoma type, stages I and II, in a human subject; comprised of: (a) determining, in a tumor sample (biopsy) from the human subject, the levels of expression of the microRNAs hsa-miR-223, hsa-miR-103, hsa-miR-107, hsa-miR-425, hsa-miR-340, hsa-miR-130b, hsa-miR-652, hsa-miR-214, and hsa-miR-204; (b) determining a value which depends on the levels of expression of the microRNAs; and (c) determining the risk of relapse in renal cancer of the clear cell renal carcinoma type, in stages I and II, in the said human subject, by comparing the value obtained in step (b) with a cut-off value.

This disclosure relates to a composition for diagnosing cancer by using potassium channel proteins; to a kit for diagnosing cancer comprising the composition; and to an information providing method for diagnosing cancer. Specifically, the composition or kit for diagnosing cancer provided in this disclosure may be used to diagnose the onset of cancer regardless of its type, by measuring the expression levels of potassium channels, KCa3.1 channel and KCa2.3 channel, or a regulator thereof from vascular endothelial cells treated with a sample of a subject, or from red blood cells isolated from the subject, and thus can be widely utilized in determining the stages of progression (growth, metastasis, prognosis, and recurrence) of various cancers.

The invention provides a method of treating a tumor in a human patient comprising (i) identifying a patient as having a LAG-3 positive tumor and (ii) administering to the patient a PD-1 pathway inhibitor, a combination of a PD1 pathway inhibitor and an immune checkpoint inhibitor, a combination of a LAG-3 inhibitor and a PD-1 pathway inhibitor, or an anti-CTLA4 antibody. In some embodiments, the method further comprises identifying the patient as having a LAG-3 positive PD-Ll positive tumor. In some embodiments, the LAG-3 inhibitor is an anti-LAG-3 antibody and the PD-1 pathway inhibitor is an anti-PD-1 antibody. The methods of the invention can improve response rates to treatment with a PD-1 pathway inhibitor, a combination of a PD1 pathway inhibitor and an immune checkpoint inhibitor, or a combination of a LAG-3 inhibitor and a PD-1 pathway inhibitor.

The use of differentiation marker CD32 for the detection of cellular reservoirs of a mammalian immunodeficiency virus. Also the use of the differentiation marker CD32 for making a prognosis, diagnosing a remission, and evaluating the efficacy of treatment of the mammalian immunodeficiency. A multi-specific antibody that recognizes both at least one epitope of CD32 and at least one characteristic of the lymphocyte cells, a composition including the antibody, and the use of the antibody in treatment.

The present invention is related to detecting respiratory diseases using molecular markers as prognostic tool of the evolution of respiratory infection cases. Concretely, during the differential diagnostic of respiratory infections caused by the Syncytial Respiratory Virus and human Metapneumovirus, it will be established the expression pattern of the severity markers of IL-3, IL-33 and IL12p40. The expression pattern of the molecular markers can be defined in biological samplers using ELISA assays, flow cytometry or PCR in real time. The confirmation of the etiological agent of the infection in combination to the pattern definition of the molecular markers IL-3, IL-33 and IL12p40 will indicate a prognostic of the disease severity.

Certain embodiments of the present invention relate to methods and products for use in the determination of treatment of rheumatoid arthritis (RA). Particularly, although not exclusively, embodiments of the present invention relate to predicting the likelihood of a patient suffering from rheumatoid arthritis maintaining remission following cessation of disease-modifying anti-rheumatic drugs (DMARDs). Certain embodiments of the present invention are based on the determination of certain biomarkers of drug-free remission in RA following cessation of DMARD therapy.