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34 results about "P53 expression" patented technology
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P53 is a transcriptional activator, regulating the expression of Mdm2 (for its own regulation) and the genes involved in growth arrest, DNA repair and apoptosis. Some important examples are listed below. Growth arrest: p21, Gadd45, and 14-3-3s.
Cancer immunotherapy incorporating p53
InactiveUS20060153808A1BiocidePeptide/protein ingredientsAbnormal tissue growthChemotherapeutic drugs
A method of stimulating an immune response to a tumor in an immunocompetent subject by administering a p53 expression construct to a tumor. The construct expresses p53 in tumor cells in an amount sufficient to stimulate an immune response against the tumor. Both viral and non-viral delivery systems are contemplated. The method can be combined with chemotherapy agents as well as with other cancer therapies.
Owner:INTROGEN THERAPEUTICS INC +1
BIS(ARYLMETHYLIDENE)ACETONE COMPOUND, ANTI-CANCER AGENT, CARCINOGENESIS-PREVENTIVE AGENT, INHIBITOR OF EXPRESSION OF Ki-Ras, ErbB2, c-Myc AND CYCLINE D1, BETA-CATENIN-DEGRADING AGENT, AND p53 EXPRESSION ENHANCER
ActiveUS20100152493A1Growth inhibitionPrevent cancerOrganic chemistryAntineoplastic agentsSolubilityCancer cell
It has been demanded to improve the poor solubility of curcumin to develop an anti-tumor compound capable of inhibiting the growth of various cancer cells at a low concentration. Thus, disclosed is a novel synthetic compound, a bis(arylmethylidene)acetone, which has both of an excellent anti-tumor activity and a chemo-preventive activity. A bis(arylmethylidene)acetone (i.e., a derivative having a curcumin skeleton) which is an anti-tumor compound and has a chemo-preventive activity is synthesized and screened. A derivative having enhanced anti-tumor activity and chemo-preventive activity can be synthesized.
Owner:SHIBATA HIROYUKI
Inhibition of pulmonary fibrosis with nutlin-3A and peptides
ActiveUS9630990B2Effective treatmentPolypeptide with localisation/targeting motifOrganic active ingredientsCell-Extracellular MatrixECM Protein
In fibrotic lung fibroblasts, basal levels of p53 protein (and miR-34a) are markedly suppressed, leading to reduced p53-mediated inhibition of uPA and uPAR, or concurrent induction of PAI-1. These changes contribute to excessive FL-fibroblast proliferation and production of extracellular matrix (ECM), and, therefore, pulmonary fibrosis. These processes are reversed by treating the cells, and treating subjects suffering from idiopathic pulmonary fibrosis (IPF) with the small organic molecule nutlin-3a (NTL) or with a peptide, CSP-4 (SEQ ID NO:1), or variants or derivatives or multimers of this peptide, which increase p53 levels by inhibiting MDM2-mediated degradation of p53 protein. Use of these compounds serves as a new approach to the treatment of IPF, they restore p53 expression and p53-mediated changes in the uPA-fibrinolytic system in FL-fibroblasts and restrict production and deposition of ECM.
Owner:BOARD OF RGT THE UNIV OF TEXAS SYST
Peptide Inhibition of Lung Epithelial Apoptosis and Pulmonary Fibrosis
ActiveUS20090227515A1High expressionBlock bleo induced mouse lung fibrosisPolypeptide with localisation/targeting motifCell receptors/surface-antigens/surface-determinantsIn vivoPulmonary fibrosis
During lung injury, p53 expression increases, inducing plasminogen activator inhibitor-1 (PAI-1) while inhibiting expression of urokinase-type plasminogen activator (uPA) and its receptor (uPAR), resulting in apoptosis of lung epithelial cells (LECs). In the bleomycin lung injury model, p53 and PAI-1 are induced while uPA and uPAR are inhibited. A 20 residue peptide DGIWKASFTTFTVTKYWFYR termed PP-1 (the Cav-1 scaffolding domain) or peptide NYHYLESSMTALYTLGH, termed PP-2, protected LECs from bleomycin-induced apoptosis in vitro and in vivo and prevented subsequent pulmonary fibrosis by attenuating lung epitheilial damage. Pharmaceutical compositions, peptide multimers and deliverable polypeptides comprising the above peptides are dislcosed. The peptides and functional variants, peptide multimers, cell-targeted polyepeptides and pharmaceutical compositions are used in methods for inhibiting apoptosis of injured or damaged lung epithelial cells and for treating acute lung injury and consequent pulmonary fibrosis.
Owner:BOARD OF RGT THE UNIV OF TEXAS SYST
Methods and compositions for the diagnosis and treatment of cancer
Methods for the treatment of squamous cell carcinoma using a p53-expressing viral vector are disclosed. In particular embodiments, the vector is a replication-deficient adenovirus. In addition, there are provided methods for examining the development and treatment of microscopic residual disease in the context of post-surgical environments and in body cavities.
Owner:CLAYMAN GARY
Peptide inhibition of lung epithelial apoptosis and pulmonary fibrosis
ActiveUS8697840B2High expressionPolypeptide with localisation/targeting motifCell receptors/surface-antigens/surface-determinantsZymogenReceptor
During lung injury, p53 expression increases, inducing plasminogen activator inhibitor-1 (PAI-1) while inhibiting expression of urokinase-type plasminogen activator (uPA) and its receptor (uPAR), resulting in apoptosis of lung epithelial cells (LECs). In the bleomycin lung injury model, p53 and PAI-1 are induced while uPA and uPAR are inhibited. A 20 residue peptide DGIWKASFTTFTVTKYWFYR termed PP-1 (the Cav-1 scaffolding domain) or peptide NYHYLESSMTALYTLGH, termed PP-2, protected LECs from bleomycin-induced apoptosis in vitro and in vivo and prevented subsequent pulmonary fibrosis by attenuating lung epitheilial damage. Pharmaceutical compositions, peptide multimers and deliverable polypeptides comprising the above peptides are dislcosed. The peptides and functional variants, peptide multimers, cell-targeted polyepeptides and pharmaceutical compositions are used in methods for inhibiting apoptosis of injured or damaged lung epithelial cells and for treating acute lung injury and consequent pulmonary fibrosis.
Owner:BOARD OF RGT THE UNIV OF TEXAS SYST
Use of Soluble Galectin-3 (Gal-3) for Cancer Treatment
InactiveUS20100330602A1Modulate interactionImprove cell-cellPeptide/protein ingredientsMicrobiological testing/measurementTumor targetCancer cell
The present invention provides a method for preventing or treating cancer or tumorgenesis disorder comprising administering a prevention or treatment effective amount of a p53 mediated secretome component, such as Gal-3, to a patient in need thereof, thereby preventing or treating cancer or tumorgenesis disorders. Compositions and methods useful for modulating the secretome, including Gal-3, of a cell, comprising increasing extracellular levels of Gal-3, p53 expression, or expression of a downstream effector of p53, in the cell are also provided. Furthermore, methods for identifying tumor targets, diagnostic or prognostic indicators, and therapeutic strategies comprising determining extracellular levels of secreted proteins or secretomes, including Gal-3 are also provided. The present invention provides a novel tumor suppressive mechanism of p53 involving paracrine induction of apoptosis through extracellular Gal-3 levels. The invention also provides evidence that cancer cells are more susceptible to the treatment than normal cells, suggesting augmented expression of the receptor component to Gal3.
Owner:EMORY UNIVERSITY
METHOD FOR MAINTAINING INCREASED INTRACELLULAR p53 LEVEL, INDUCED BY PLATINUM-BASED ANTICANCER DRUG, AND APPLICATION THEREOF
InactiveUS20200009185A1Effectively death of cancer cellMinimize side effectsHeavy metal active ingredientsOrganic active ingredientsIntracellularUbiquitin ligase
The present invention relates to a method for maintaining the increased intracellular p53 level, induced by a platinum-based anticancer drug, and an application thereof and, more specifically, to a method for maintaining the increased intracellular p53 level in cells by administering a platinum-based anticancer drug and siRNA to ubiquitin ligase for p53 to a subject in need thereof in combination and sequentially, and a composition for promoting cancer cell apoptosis using the same.According to the method of the present invention, the increased intracellular p53 expression level can be maintained for a long period of time in spite of the treatment with a low-concentration platinum-based anticancer drug, thereby effectively inducing the apoptosis of cancer cells and minimizing the drug side effect caused by the administration of the platinum-based anticancer drug, and thus the present invention can be favorably used in the prevention of cancer or the development of cancer medicines.
Owner:ENHANCEDBIO INC
A kind of cultivation method for transfecting human tumor suppressor gene green fluorescent protein carrier
InactiveCN102286488AStrong replicabilityImprove expression efficiencyMicrobiological testing/measurementGenetic engineeringRestriction enzyme digestionRNA extraction
A method for the cultivation of human tumor suppressor gene green fluorescent protein carrier, design primers on GENBANK with reference to human anti-cancer gene sequence, collect peripheral blood of early lung cancer patients to extract total RNA, and use reverse transcription polymerase chain reaction (RT-PCR) Amplify the P53 fragment, clone the gene fragment directionally onto the pMD18-T vector, construct the pMD18-P53 recombinant plasmid, identify the recombinant plasmid by PCR amplification, enzyme digestion and sequencing, and digest the pMD18-P53 Identify and extract the directional clone of the P53 target gene into the pEGFP-N1 eukaryotic expression vector to construct the pEGFP-N1-P53 expression vector. The beneficial effects of the present invention are: using the eukaryotic expression vector pEGFP-N1, which is safe, stable, strong in replication, high in expression rate, and easy to detect, as the transport carrier of human anti-cancer genes, thereby constructing a safe, stable, easy-to-detect, safe and reliable The eukaryotic expression vector pEGFP-N1-P53 is used for the prevention and treatment of cancer.
Owner:HENAN UNIV OF SCI & TECH
Inhibition of pulmonary fibrosis with nutlin-3a and peptides
ActiveUS20160272678A1Prevent proliferationEffective treatmentPolypeptide with localisation/targeting motifOrganic active ingredientsCell-Extracellular MatrixECM Protein
In fibrotic lung fibroblasts, basal levels of p53 protein (and miR-34a) are markedly suppressed, leading to reduced p53-mediated inhibition of uPA and uPAR, or concurrent induction of PAI-1. These changes contribute to excessive FL-fibroblast proliferation and production of extracellular matrix (ECM), and, therefore, pulmonary fibrosis. These processes are reversed by treating the cells, and treating subjects suffering from idiopathic pulmonary fibrosis (IPF) with the small organic molecule nutlin-3a (NTL) or with a peptide, CSP-4 (SEQ ID NO:1), or variants or derivatives or multimers of this peptide, which increase p53 levels by inhibiting MDM2-mediated degradation of p53 protein. Use of these compounds serves as a new approach to the treatment of IPF, they restore p53 expression and p53-mediated changes in the uPA-fibrinolytic system in FL-fibroblasts and restrict production and deposition of ECM.
Owner:BOARD OF RGT THE UNIV OF TEXAS SYST
Combination of Ad-P53 and Chemotherapy for the Treatment of Tumours
InactiveUS20080293652A1Treat cancerOrganic active ingredientsPeptide/protein ingredientsRecurrent CancerChemotherapy combinations
The present invention relates to the use of p53 gene therapy to treat recurrent cancers in combination with a radio- or chemotherapy. Patients with recurring cancers are treated with a p53 expression construct followed by subsequent radio- or chemotherapy treatment. Viral and non-viral delivery systems, as well as various radio- and chemotherapy regimens are disclosed.
Owner:INTROGEN THERAPEUTICS INC
Antihelminthic drugs as a treatment for hyperproliferative diseases
The present invention is directed to the use of benzimidazole derivatives for the treatment of tumors and in combination with tumor suppressor gene therapy. In a particular embodiment, treatment of p53-positive tumors with benzimidazole derivatives induces p53 expression and increases its half-life, resulting in apoptotic death of the tumor cells. Similarly, in conjunction with p53 gene therapy, benzimidazole derivatives induce p53 expression and accumulation in tumor cells regardless of their p53 status. The combination treatment subsequently elicits apoptosis of the tumor cells.
Owner:INTROGEN THERAPEUTICS INC +1
Use of hades as tumor suppressor target
InactiveUS20130157959A1High expressionMechanism is preventedPeptide/protein ingredientsMicrobiological testing/measurementSuppressorP53 expression
The present invention relates to a new use of Hades as a tumor suppressor target, more particularly to a composition for suppressing tumor comprising an expression or action inhibitor of Hades protein having an amino acid sequence of SEQ ID NO: 2 as an effective ingredient. The present inventors have found that the overexpressed Hades protein interacts with p53 to inhibit the exonuclear mechanism of p53 and the knowdown of Hades induces increase in the expression of p53, demonstrating that Hades is a negative regulator to p53. Therefore, it would be understood that the inhibition of Hades overexpressed in tumor cells contributes to tumor-supressive effects of p53. The drug candidates capable of modulating the expression of the Hades protein, inhibiting the actions of the Hades protein or inhibiting interecation between Hades and p53 are considered a promising anticancer drug.
Owner:KONKUK UNIV IND COOP CORP
Pharmaceutical combination comprising a cip2a silencing agent for use in the treatment of a hyperproliferative disorder, preferably one with impaired p53 function
The invention is based on a finding that silencing CIP2A (KI-AA1524) gene sensitizes cancer cells for apoptosis-inducing activity of certain small molecule chemotherapeutic agents. Thus, the invention is directed to a respective combination therapy, sensitization method and pharmaceutical compositions. The invention further relates to a method of selecting cancer therapy for a subject on the basis of CIP2A and p53 expression and / or protein activity in a sample obtained from said subject.
Owner:TURUN YLIOPISTO
P53 treatment of papillomavirus and carcinogen-transformed cells in hyperplastic lesions
Methods for the prevention, suppression, and inhibition of growth of a papilloma-virus transformed cell in a hyperplastic lesion using a topically applied p53 expression cassette are disclosed. In addition, there are provided pharmaceutical preparations of a p53 expression cassette suitable for topical delivery to a papillomavirus-transformed cell in a hyperplastic lesion.
Owner:INTROGEN THERAPEUTICS INC
P53 silenced endothelial progenitor cells for diabetes
ActiveUS10016458B2Reducing （or eliminating） cellReduce impactBiocideGenetic material ingredientsProgenitorDiabetes mellitus
Owner:BAYSTATE HEALTH
Cell strain capable of inducing and realizing dual-stabilization of P53 expression and construction method and application thereof
InactiveCN102168069AGenetic material ingredientsMammal material medical ingredientsMechanism of actionCell strain
The invention relates to the field of biological medicine, in particular to a cell strain capable of inducing and realizing dual-stabilization of P53 expression and a construction method and application thereof. As for the cell strain capable of inducing and realizing the dual-stabilization of the P53 expression, the cell strain U-2OSE6tet6 was collected in China Center for Type Culture Collection on August 12, 2010, and the collection number is CCTCC No: C201075. Experiments prove that the cell strain U-2OSE6tet6 capable of inducing and realizing the dual-stabilization of the P53 expression can indirectly change the P53 content in U-2OSE6tet6 cells by regulating the expression of an E6 gene through doxycycline, and provide an experimental platform for studying relevant action mechanism of the P53 of screening medicaments for treating osteosarcoma.
Owner:SECOND AFFILIATED HOSPITAL ZHEJIANG UNIV COLLEGE OF MEDICINE
Bis(arylmethylidene)acetone compound, anti-cancer agent, carcinogenesis-preventive agent, inhibitor of expression of Ki-Ras, ErbB2, c-Myc and Cycline D1, β-catenin-degrading agent, and p53 expression enhancer
It has been demanded to improve the poor solubility of curcumin to develop an anti-tumor compound capable of inhibiting the growth of various cancer cells at a low concentration. Thus, disclosed is a novel synthetic compound, a bis(arylmethylidene)acetone, which has both of an excellent anti-tumor activity and a chemo-preventive activity. A bis(arylmethylidene)acetone (i.e., a derivative having a curcumin skeleton) which is an anti-tumor compound and has a chemo-preventive activity is synthesized and screened. A derivative having enhanced anti-tumor activity and chemo-preventive activity can be synthesized.
Owner:SHIBATA HIROYUKI
Pharmaceutical combination comprising a cip2a silencing agent for use in the treatment of a hyperproliferative disorder, preferably one with impaired p53 function
Owner:TURUN YLIOPISTO
Application of p53 expression product in preparing medicine for treating tumor
InactiveCN101143222AIncrease lethalityStrong targetingPeptide/protein ingredientsGenetic material ingredientsTumor therapyTumor cell apoptosis
The invention belongs to the biomedical field and relates to the application of p53 in preparing for a drug preparation for remedying the tumor. A p53 gene coding product is a transcription regulator which can induce the apoptosis or the block of the cell cycle by regulating lower target gene. An over-expression of the p53 can very effectively induce the apoptosis of tumor cells. Attenuated salmonella typhimurium can be used as a carrier to introduce the p53 to express inside the tumor cells and kill the tumor cells. The development of a novel treatment drug which considers the salmonella with the p53 as orally taken gene not only solves the problem of non-injection path of a protein polypeptide drug but also more importantly provides the tumor treatment with a safe, effective, peculiar and economical method.
COP1 molecules and uses thereof
Owner:GENENTECH INC
Pharmaceutical combination comprising a CIP2A silencing agent for use in the treatment of a hyperproliferative disorder, preferably one with impaired p53 function
The invention is based on a finding that silencing CIP2A (KI-AA1524) gene sensitizes cancer cells for apoptosis-inducing activity of certain small molecule chemotherapeutic agents. Thus, the invention is directed to a respective combination therapy, sensitization method and pharmaceutical compositions. The invention further relates to a method of selecting cancer therapy for a subject on the basis of CIP2A and p53 expression and / or protein activity in a sample obtained from said subject.
Owner:TURUN YLIOPISTO
Cell strain capable of inducing and realizing dual-stabilization of P53 expression and construction method and application thereof
InactiveCN102168069BGenetic material ingredientsMammal material medical ingredientsMechanism of actionCell strain
The invention relates to the field of biological medicine, in particular to a cell strain capable of inducing and realizing dual-stabilization of P53 expression and a construction method and application thereof. As for the cell strain capable of inducing and realizing the dual-stabilization of the P53 expression, the cell strain U-2OSE6tet6 was collected in China Center for Type Culture Collection on August 12, 2010, and the collection number is CCTCC No: C201075. Experiments prove that the cell strain U-2OSE6tet6 capable of inducing and realizing the dual-stabilization of the P53 expression can indirectly change the P53 content in U-2OSE6tet6 cells by regulating the expression of an E6 gene through doxycycline, and provide an experimental platform for studying relevant action mechanism of the P53 of screening medicaments for treating osteosarcoma.
Owner:SECOND AFFILIATED HOSPITAL ZHEJIANG UNIV COLLEGE OF MEDICINE
Variant p53 gene and recombinant adenovirus for cancer treatment
The invention discloses a variant p53 gene for cancer treatment. A cDNA base sequence of the p53 gene is constructed by replacing codon 72 in a cDNA base sequence of a naturally occurring p53 gene with a target codon. The invention also discloses a recombinant adenovirus containing the variant p53 gene. The recombinant adenovirus is constructed by artificially synthesizing a DNA target fragment containing the target codon, replacing the DNA target fragment with a DNA fragment containing a p53 expression cassette in an intermediate plasmid to generate a variant intermediate plasmid containing the variant p53 gene, and introducing the DNA fragment containing the variant p53 gene in the variant intermediate plasmid into a shuttle plasmid, and then performing homologous recombination to obtainthe recombinant adenovirus containing the variant p53 gene.
Owner:SYNO SHENZHEN BIOMEDICAL RES CO LTD
CARDIAC PROGENITOR CELLS HAVING ENHANCED p53 EXPRESSION AND USES THEREOF
Disclosed herein are compositions comprising cardiac progenitor cells that express exogenous p53 protein. Such compositions are useful for treating cardiac diseases or disorders. Also disclosed herein are methods of producing cardiac progenitor cells that express exogenous p53.
Owner:AAL SCI INC
METHOD FOR MAINTAINING INCREASED INTRACELLULAR p53 LEVEL, INDUCED BY PLATINUM-BASED ANTICANCER DRUG, AND APPLICATION THEREOF
InactiveUS20180153932A1Effectively death of cancer cellMinimize side effectsOrganic active ingredientsHeavy metal active ingredientsCancer preventionPlatinum
The present invention relates to a method for maintaining the increased intracellular p53 level, induced by a platinum-based anticancer drug, and an application thereof and, more specifically, to a method for maintaining the increased intracellular p53 level in cells by administering a platinum-based anticancer drug and siRNA to ubiquitin ligase for p53 to a subject in need thereof in combination and sequentially, and a composition for promoting cancer cell apoptosis using the same.According to the method of the present invention, the increased intracellular p53 expression level can be maintained for a long period of time in spite of the treatment with a low-concentration platinum-based anticancer drug, thereby effectively inducing the apoptosis of cancer cells and minimizing the drug side effect caused by the administration of the platinum-based anticancer drug, and thus the present invention can be favorably used in the prevention of cancer or the development of cancer medicines.
Owner:ENHANCEDBIO INC
An application of promoting atg5-atg12 conjugation to enhance autophagy by scavenging wild-type p53 protein
ActiveCN114381461BInhibition of conjugation formationIncreased autophagy levelsP53 proteinFermentationDrug targetBiochemistry
Owner:ACADEMY OF MILITARY MEDICAL SCI
METHOD FOR MAINTAINING INCREASED INTRACELLULAR p53 LEVEL, INDUCED BY PLATINUM-BASED ANTICANCER DRUG, AND APPLICATION THEREOF
InactiveCN109475644AUseful for developmentEfficient induction of killingInorganic active ingredientsGenetic material ingredientsPlatinumSide effect
Owner:SILVERHAND BIOTECH
Method for preventing or treating tuberculosis by a P53 expression regulating composition for M. tuberculosis control in cells and the use thereof
The present invention relates to a pharmaceutical composition for preventing or treating tuberculosis comprising compound (K279-1558) as an active ingredient. Compound (K279-1558) which is an active ingredient of the present invention has an effect of inhibiting the proliferation of M. tuberculosis by inducing apoptosis of macrophages infected with tuberculosis through the overexpression of p53. Therefore, the method of the present invention comprising said compound as an active ingredient could be usefully used for preventing or treating tuberculosis.
Owner:THE IND & ACADEMIC COOP IN CHUNGNAM NAT UNIV (IAC)
Gene recombined medicine of adenovirus carrier and p53 gene for treating proliferative diseases
InactiveCN1327899CTo achieve the purpose of treatmentPeptide/protein ingredientsGenetic material ingredientsHuman tumorConfusion
A kind of recombinant gene medicine of adenovirus vector and gene p53 which can treat proliferative diseases is a confusion sequence constructed from adenovirus vector and human tumor inhibition gene p53 expression kit. In the present invention, we made homologous recombination of adenovirus vector with human gene p53 in procaryotic cells (E. coli), then obtained the recombinant gene medicine of adenovirus vector and human gene p53 expression kit. The human p53 gene expression kit is a characteristic sequence consisting of promoter-p53 cDNA-polyadenine nucleotide. The medicine can be used to prepare clinic gene therapeutic products for treating proliferative disease such as cheloid.
Owner:深圳市赛百诺基因技术有限公司
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