Abstract:
The present invention relates to a pharmaceutical composition for preventing or treating cancer comprising a PIP4K2C inhibitor as an active ingredient. The present invention provides a composition for efficient and radical treatment of cancer by discovering PIP4K2C as a new treatment target for cancer, which exhibits a high recurrence rate and is difficult to radically treat, and selecting a drug that inhibits PIP4K2C among known anticancer drugs.
Abstract:
A method for estimating a toxicity level of radiation therapy on a patient comprises characterizing radiosensitivity of a cell sample from the patient to ionizing radiation to determine a first radiosensitivity factor by biochemical analysis. The first radiosensitivity factor is determined by biochemical analysis of a sample collected from the patient under examination in a basal state, to quantify a marker or a combination of markers. Dosimetric data is analyzed using data originating from treatment planning to determine a second treatment factor. The level of toxicity is determined by a combination of the first radiosensitivity factor and the second treatment factor. The method may be used to assess the risk factors of a radiation therapy treatment on a patient suffering from, for example, cancer to determine whether the patient will be able to tolerate further radiation without there being a major, or even lethal, toxicological risk.
Abstract:
Methods and compositions are provided for treating breast cancer in patients with a PI3K inhibitor, GDC-0941 in combination with an endocrine therapy agent.
Abstract:
A method of quantifying ammonia, which method includes: performing a first reaction in which a test liquid containing ammonia is reacted with ATP and L-glutamic acid in the presence of glutamine synthetase to produce ADP; performing a second reaction in which the produced ADP is reacted with glucose in the presence of ADP-dependent hexokinase to produce glucose-6-phosphate; performing a third reaction in which the produced glucose-6-phosphate is reacted with an oxidized NAD compound in the presence of glucose-6-phosphate dehydrogenase to produce a reduced NAD compound; and quantifying the reduced NAD compound to quantify ammonia.
Abstract:
An antibody has as a target molecule a ubiquitin protein comprising a phosphorylated serine residue at position 65. In addition, a method is provided for specifically detecting Parkinson's disease at an early stage, in which a target molecule is a ubiquitin protein comprising a phosphorylated serine residue at position 65, a pharmaceutical composition for definitively treating or preventing Parkinson's disease, and a method for screening for the pharmaceutical composition.
Abstract:
The present invention relates to methods of treating or preventing a metabolic disorder in a subject, methods of treating or preventing coronary artery disease in a subject with a metabolic disorder, as well as methods of reducing hepatic glucose production in a subject. Such methods include, but are not limited to, the administration to the subject of inhibitors or activators of CaMKII, IP3Rs, calcineurin, p38, MK2/3, HDAC4, Dach1, Dach2, or any combination thereof. The invention also provides methods of identifying a compound that inhibits the activity of CaMKII, IP3Rs, calcineurin, p38, MK2/3, HDAC4, Dach1 or Dach2, or reduces the activity and/or activation of CaMKII, IP3Rs, calcineurin, p38, MK2/3, HDAC4, Dach1 or Dach, or activates CaMKII, IP3Rs, calcineurin, p38, MK2/3, HDAC4, Dach1 or Dach2.
Abstract:
Disclosed herein are new prognostic molecular markers for prostate cancer. More specifically, the invention has identified that overexpression or amplification of at least one of AURKA or MYCN define a distinct subgroup of prostate cancer that is predisposed to the development of lethal NEPC, who will benefit from early intervention.
Abstract:
Natural-KilleifT-Cell Lymphoma (NKTCL) susceptibility prediction, diagnosis and therapy. The invention relates to a method for predicting Natural Killer T-cell Lymphoma (NKTCL) susceptibility and/or diagnosing NKTCL in a subject comprising testing for JAK mutations. The invention also relates to a method of screening for candidate agents capable of treating NKTCL using a cell line comprising at least one JAK mutation. The invention includes an NKTCL animal model comprising at least one JAK mutation. The invention also includes JAK inhibitors for treating NKTCL.
Abstract:
Provided herein are methods of inducing differentiation of a mammalian myoblast into a mammalian myocyte that include contacting a mammalian myoblast with an oligonucleotide that decreases Mitogen-activated protein kinase kinase kinase kinase 4 (Map4k4) mRNA expression in a mammalian myoblast or myocyte. Also provided are methods of inducing mammalian myoblasts or myocytes to form a myotube that include contacting two or more mammalian myoblasts or two or more mammalian myocytes with an oligonucleotide that decreases Map4k4 mRNA expression in a mammalian myoblast or myocyte. Also provided are methods of identifying a candidate agent useful for inducing muscle formation, and compositions containing an oligonucleotide that decreases Map4k4 mRNA expression in mammalian myoblast or myocyte and one or more additional muscle therapeutic agents and/or muscle-building neutraceuticals.
Abstract:
The invention provides to PIK3C2G (phosphatidylinositol-4-phosphate 3-kinase, catalytic subunit type 2 gamma) gene fusions and PIK3C2G fusion proteins. The invention further provides methods of diagnosing and treating diseases or disorders associated with PK3C2G fusions, such as conditions mediated by aberrant PIK3C2G expression or activity, or conditions associated with overexpression of PIK.3C2G.