33 results about "P53 pathway" patented technology

The present invention provides a method of improving the efficiency of establishment of induced pluripotent stem (iPS) cells, comprising inhibiting the p53 function in the step of somatic cell nuclear reprogramming. The inhibition of p53 function is achieved by bringing a substance selected from the group consisting of (1) chemical inhibitors of p53, (2) dominant negative mutants of p53 and nucleic acids that encode the same, (3) siRNAs and shRNAs against p53 and DNAs that encode the same, and (4) p53 pathway inhibitors, into contact with a somatic cell, and the like. The present invention also provides an agent for improving the efficiency of establishment of iPS cells, the agent comprising an inhibitor of p53 function, particularly (1) chemical inhibitors of p53, (2) dominant negative mutants of p53 and nucleic acids that encode the same, (3) siRNAs and shRNAs against p53 and DNAs that encode the same, and (4) p53 pathway inhibitors. The present invention further provides a method of producing an iPS cell, comprising bringing a nuclear reprogramming substance and an inhibitor of p53 function into contact with a somatic cell.

A pharmaceutical composition for anti-viral cancer treatment in mammals, comprising a therapeutically effective amount of Anisomelic acid or salts thereof. The pharmaceutical composition may comprise Anisomelic acid or salt thereof in an oil-in-water emulsion, for example in an isotropic mixture of at least one oil and at least one surfactant or, alternatively, in a hydrophilic solvent and a co-solvents or surfactant or a combination thereof. A method of treating or preventing of cancer in a mammal, wherein the p53 pathway is deregulated by viral oncoproteins, is also provided.

The invention presents methods of identifying small molecule compounds that are activators of tumor suppressor protein p53 pathway, and its associated family members p63 and p73, function. The invention is further drawn to methods of killing tumor cells and treating cancers or other conditions requiring activation of the p53 family member pathways and DNA damage response pathways with the small molecules.

Human CHD genes are identified as modulators of the p53 pathway, and thus are therapeutic targets for disorders associated with defective p53 function. Methods for identifying modulators of p53, comprising screening for agents that modulate the activity of CHD are provided.

The invention presents methods of identifying small molecule compounds that are activators of tumor suppressor protein p53 pathway, and its associated family members p63 and p73, function. The invention is further drawn to methods of killing tumor cells and treating cancers or other conditions requiring activation of the p53 family member pathways and DNA damage response pathways with the small molecules.

It has now been found that the p53 pathway is inactivated in ocular cancers such as retinoblastoma. As such, the present invention is a method for inducing ocular cancer cell death using a p53 activator. In particular embodiments, the p53 activator blocks the interaction between DM2 or DMX and p53. As the p53 activator induces ocular cancer cell death, a method for preventing or treating ocular cancer is also provided.

The application of theabrownin in the preparation of drugs for treating liver cancer belongs to the technical field of theabrownin use. Specifically include: the application of theabrownin in the preparation of drugs for treating liver cancer, theabrownin promotes the apoptosis of hepatocellular carcinoma Huh7 cells by activating the JNK signaling pathway, and inhibits the growth of liver cancer xenografts. The present invention proves through various tests that theabrownin has significant anti-proliferation and pro-apoptotic effects on Huh7 cells, and has dose-dependent effects. Theabrownin promotes the apoptosis of Huh7 cells and inhibits the growth of zebrafish liver cancer xenografts by activating the JNK signaling pathway. Theabrownin can inhibit tumor by 48.1%. Moreover, theabrownin regulates downstream apoptosis-related genes by activating the P53 pathway PUMA, NOXA, Bax, and Bcl‑2 and so on to promote the apoptosis of P53 wild Sk‑hep1 cells.

The present disclosure relates to a method of inducing apoptosis in a cancer cell by delivery of exogenous Coenzyme Q1O or its metabolites thereof in a pharmaceutically acceptable carrier to effectuate cell contact of endogenous Coenzyme Q1O or its metabolites thereof in addition to but not limited to mevalonic acid and oleic acid to form an intracellular complex. The present disclosure also provides a method of modulating the p53 pathway and Bcl-2 protein family in a manner that restores the apoptotic potential to a cancer cell by delivery of Coenzyme Q1O in a pharmaceutically acceptable carrier. The present disclosure further provides a method to specifically normalize the ratio of pro-apoptotic and anti-apoptotic members of the Bcl-2 gene family in a proportion to re-program a cancer cell to undergo apoptosis.

Human LCE genes are identified as modulators of the p53 pathway, and thus are therapeutic targets for disorders associated with defective p53 function. Methods for identifying modulators of p53, comprising screening for agents that modulate the activity of LCE are provided.

The invention includes compositions comprising NSC59984 or a derivative or analogue thereof and a pharmaceutically acceptable carrier. The invention further includes methods of treating or preventing cancer in a subject, comprising the step of administering to the subject the compositions contemplated within the invention.

Provided herein are methods of treating a cognitive deficit, including cognitive deficits associated with a Fmr1 genetic defect. More particularly, provided herein are methods in which an effective amount of a MDM2-p53 pathway inhibitor is administered to a subject afflicted with at least one cognitive deficit, whereby administration of the inhibitor improves, enhances, or rescues at least one cognitive deficit in the subject.