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.

The present invention provides a new approach for cancer treatment by utilizing gene therapy combined with radiation therapy to enhance cytotoxicity in malignant cells. Specifically, the present invention demonstrates that molecular chemotherapy with the cytosine deaminase gene and 5-fluorocytosine is an effective radiosensitizing strategy which may lead to substantial improvement in tumor control, with less normal tissue toxicity than conventional systemic administration of 5-fluorouracil, that would translate into improved cure rates and better survival. A noninvasive method is described for continuous in vivo monitoring of 5-fluorouracil production via magnetic resonance spectroscopy. An adenovirus encoding cytosine deaminase gene which selectively replicates in tumor cells with a defective p53 pathway was constructed. Also provided is an adenovirus which encodes a fusion protein of cytosine deaminase and uracil phosphoribosyltransferase.

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 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.

The invention discloses a medicine for treating or preventing human cervical cancer as well as a preparation method and application thereof, belongs to the technical field of medicines, and particularly relates to a medicine for treating or preventing human cervical cancer based on an MDM2-p53 protein and protein interaction signal channel and a target mechanism as well as a preparation method and application thereof. The invention finds that the action mechanism of the compound 1, 5, 6-trimethoxy-2, 7-dihydroxyphenanthrene is a new mechanism based on an MDM2-p53 protein and protein interaction signal pathway and a target spot. The medicine disclosed by the invention has the characteristics of novel action mechanism, no addiction and small dosage, and has the effect of inhibiting the growth of Hela cells. The IC50 on Hela cells for 48 hours is 0.42 [mu]M. And cell apoptosis can be caused by acting on an MDM2-p53 pathway, and meanwhile, mitochondrial apoptosis is caused.

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.

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 relates to an application of Exenatide in the preparation of drugs for reversing the activation of FFA on P53, which pertains to the field of medicine. The application of the Exenatide in the preparation of the drugs for reversing the activation of FFA on the sequence specific transcription factor P53 can inhibit the increases of P53, P21 and bax mRNA expressions and the decreases of bcl-2, CyclinD1 and CyclinB2 mRNA expressions caused by FFA. The Exenatide can prevent the occurrence of type II diabetes caused by P53 pathway during the early stage of obesity.

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.

Reconstituted human breast tumor models are disclosed. The models, which are incorporated into mice, provide actual tumors that arise spontaneously, thereby mimicking naturally occurring breast cancer. The tumors are genetically human, because they arise from human mammary tissues that develop from human mammary epithelial cells implanted into host mice. Prior to implantation, the mammary epithelial cells are genetically modified to contain either: (a) a recombinant human oncogene and an SV40er; or (b) a recombinant human oncogene, a transgene or shRNA that inhibits the p53 pathway, and a transgene or shRNA that inhibits the Rb pathway.

Described herein are methods and compositions for regulation of the p53 pathway, providing intrinsic “sternness” allowing for their efficient in vitro expansion following isolation. Pharmacologic approaches to modulate p53 signaling supports expansion of stem cells, including greater clonal expansion of lung stem cells when compared to use of other small molecules such as ROCK inhibitor Y27632 alone. Effects of combined treatment with Pifithrin-α and Y27632 are additive. The current invention involves use of drugs that target the p53 pathway to reversibly regulate stem cell expansion in vitro for banking of stem cells and for pre-conditioning of stem cells prior to orthotopic transplantation.

The present invention identifies a p53 homolog gene, cep-1, and mutations thereof in the nematode C. elegans which allows for the application of molecular genetic methods to identify new components of the p53 pathway as well as genes that act in parallel to the p53 pathway. cep-1 mutants show elevated physiological germ cell death during normal development. The present invention also provides a simple system with which to perform high-throughput screens for pharmacological agents that suppress the effects of eliminating the cep-1 gene or that enhance its effectiveness when in a mutant state. This strategy should identify agents that selectively kill p53-deficient cells that are resistant to traditional chemotherapeutic regimens and thus block the formation of human tumors that arise when p53 function is compromised.

The present disclosure relates to a method of inducing apoptosis in a cancer cell by delivery of exogenous Coenzyme QlO or its metabolites thereof in a pharmaceutically acceptable carrier to effectuate cell contact of endogenous Coenzyme QlO 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 QlO 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.

The invention discloses a multi-target anti-tumor small molecule and a derivative, a preparation method, a pharmaceutical composition and application thereof. The chemical structure of the small molecule is shown as a formula I, and the derivative relates to a pharmaceutically acceptable salt of the small molecule. The small molecule and the derivative thereof have efficient tumor inhibition effects in vivo and in vitro, have low toxicity to cells and organisms, and do not generate genotoxicity; the anti-tumor activity is achieved through the multi-target effect, the HDAC inhibition activity is provided, the p53 pathway can be effectively activated, the topoisomerase activity can be effectively inhibited, and the small molecule can be used for preparing anti-tumor drugs; the preparation method is simple and easy to operate.

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.