A method for diagnosing or prognosing, multiple sclerosis including the steps of (a) measuring the amount of at least one first protein as set forth in SEQ ID NO: 1, the at least first protein belonging to the group of proteins: a first protein, a second protein, a third protein, a fourth protein and a fifth protein, as set forth in SEQ ID NO 1 to 5, (b) comparing the amount of the at least first protein with the amount of the same protein in a control sample, and (c) determining the status of the biological sample.

Methods of treating Mcl-1 dependent cancers are described herein. The methods can include determining whether the cancer is Bfl-1 positive, and administering an inhibitor of CDK9 to a patient if the cancer is Bfl-1 positive.

The diagnostic markers that provide novel diagnostic criteria to blastic plasmacytoid dendritic cell neoplasm (BPDCN) has been searched, and the presence of immunoblastoid cytomorphology, 8q24 rearrangement, and MYC expression were established as novel markers for subtyping BPDCN. It has been further found that the inhibitors which directly or indirectly inhibit the expression, functions, or signaling pathways of MYC, such as BET bromodomain-selective inhibitors or aurora kinase inhibitors, are effective in MYC-positive BPDCN, and HDAC inhibitors or BCL2 family protein inhibitors are effective as therapeutic drugs for BPDCN.

The present invention provides methods for the diagnosis of aggressive prostate cancer, including, but not limited to, methods for discerning between aggressive and non-aggressive forms of prostate cancer, and methods for detecting aggressive prostate cancer based on comparisons to a mixed control population of subjects with non-aggressive prostate cancer or not having prostate cancer.

A method of making a noninvasive molecular control and analysis is described. The method of making the noninvasive molecular control includes, predetermining a positive control for a condition of interest, selecting a cell line with a control marker for the condition of interest, amplifying release of cfDNA from the selected cell line, isolating the released cfDNA from the selected cell line, quantifying the control marker from the isolated cfDNA, determining a volume of the control marker for addition to an isolated control plasma, isolating the control plasma from a control sample, treating the isolated control plasma with a control stabilizer, determining a volume of the control plasma to add to the volume of control marker, combining the volume of the control marker with the isolated control plasma, and analyzing a sample against the noninvasive molecular control to determine the presence or absence of a condition of interest.

The disclosure concerns a method of treating complications of acute or chronic hyperglycemia and/or diet-induced obesity comprising: (i) determining whether a patient suffers from complications related to acute or chronic hyperglycemia and/or diet induced obesity, and if so, (ii) administering to the patient in need thereof a selective inhibitor of soluble TNF-α but not transmembrane TNF-α. For purposes herein, complications of acute or chronic hyperglycemia and/or diet-induced obesity include: diabetes mellitus, insulin resistance, hepatic steatosis, non-alcoholic hepatic steatosis, fibrotic liver disease, vascular disease, and chronic intestinal inflammation.

The present disclosure provides compositions and methods for the treatment of subjects having a risk of invasive breast cancer. In some embodiments, these aspects allow for the pairing of the proper treatment option for the particular subject. In some embodiments, this allows for identifying subjects who, while at risk for invasive breast cancer, will not normally respond to radiation therapy, and can instead receive an alternative therapy, such as a HER2 antibody.

The present disclosure provides compositions and methods for the treatment of subjects having a risk of invasive breast cancer. In some embodiments, these aspects allow for the pairing of the proper treatment option for the particular subject. In some embodiments, this allows for identifying subjects who, while at risk for invasive breast cancer, will not normally respond to radiation therapy, and can instead receive an alternative therapy, such as a HER2 antibody.

Provided are methods of enhancing immunogenicity of cancers. In certain aspects, the methods include administering an effective amount of a sialic acid modulator to an individual identified as having a cancer comprising dysregulated Myc. According to some aspects, the methods include administering an effective amount of a disialyl-T modulator to an individual identified as having a cancer comprising cell surface expression of disialyl-T. In certain aspects, the methods include administering an effective amount of an agent to an individual identified as having a cancer comprising cell surface expression of a glycoprotein comprising an O-glycosylated mucin-like domain, where the agent modulates the glycoprotein. Also provided are methods of assessing whether a cancer of an individual comprises dysregulated Myc.

The present invention relates to an anti-c-Met agonist antibody and use thereof, and more particularly, to an agonist antibody or fragment thereof that specifically binds to a human-derived c-Met protein, to a method for producing the same, to c-Met specific detection method using this, to a composition for preventing or treating cancer comprising the same, to a composition for inducing stem cell differentiation, and a culture medium for stem cells. The method of the present invention can be usefully used for detecting c-Met antibodies, inducing stem cell differentiation using the antibody, and treating or preventing cancer.