Search results for "MDM"

showing 10 items of 93 documents

Effects of the MDM-2 inhibitor Nutlin-3a on PDAC cells containing and lacking WT-TP53 on sensitivity to chemotherapy, signal transduction inhibitors …

2019

Abstract Mutations at the TP53 gene are readily detected (approximately 50–75%) in pancreatic ductal adenocarcinoma (PDAC) patients. TP53 was previously thought to be a difficult target as it is often mutated, deleted or inactivated on both chromosomes in certain cancers. In the following study, the effects of restoration of wild-type (WT) TP53 activity on the sensitivities of MIA-PaCa-2 pancreatic cancer cells to the MDM2 inhibitor nutlin-3a in combination with chemotherapy, targeted therapy, as well as, nutraceuticals were examined. Upon introduction of the WT-TP53 gene into MIA-PaCa-2 cells, which contain a TP53 gain of function (GOF) mutation, the sensitivity to the MDM2 inhibitor incre…

0301 basic medicineCancer ResearchNutlin-3aSettore MED/09 - Medicina Internaendocrine system diseasesmedicine.medical_treatmentmedicine.disease_causePiperazinesTargeted therapy0302 clinical medicineTP53MutationbiologyChemistryImidazolesProto-Oncogene Proteins c-mdm2OxaliplatinTargeted TherapeuticsDrug sensitivity; Nutlin-3a; Nutraceuticals; Targeted therapeutics; TP53030220 oncology & carcinogenesisMolecular MedicineMdm2NutraceuticalNutraceuticalsSignal transductionCarcinoma Pancreatic DuctalSignal Transductionmedicine.drugDrug sensitivityAntineoplastic AgentsIrinotecan03 medical and health sciencesCell Line TumorPancreatic cancerGeneticsmedicineHumansMolecular BiologyneoplasmsChemotherapymedicine.diseasedigestive system diseasesOxaliplatinPancreatic Neoplasms030104 developmental biologyCell cultureDietary Supplementsbiology.proteinCancer researchTERAPÊUTICA MÉDICATumor Suppressor Protein p53
researchProduct

HDAC1 and HDAC2 integrate the expression of p53 mutants in pancreatic cancer.

2015

Mutation of p53 is a frequent genetic lesion in pancreatic cancer being an unmet clinical challenge. Mutants of p53 have lost the tumour-suppressive functions of wild type p53. In addition, p53 mutants exert tumour-promoting functions, qualifying them as important therapeutic targets. Here, we show that the class I histone deacetylases HDAC1 and HDAC2 contribute to maintain the expression of p53 mutants in human and genetically defined murine pancreatic cancer cells. Our data reveal that the inhibition of these HDACs with small molecule HDAC inhibitors (HDACi), as well as the specific genetic elimination of HDAC1 and HDAC2, reduce the expression of mutant p53 mRNA and protein levels. We fur…

0301 basic medicineCancer ResearchProteasome Endopeptidase ComplexMutantHistone Deacetylase 2Histone Deacetylase 1Biologymedicine.disease_causeMolecular oncologyProto-Oncogene Proteins c-myc03 medical and health sciencesMicePancreatic cancerGeneticsmedicineAnimalsHumansRNA MessengerPromoter Regions GeneticMolecular BiologyRegulation of gene expressionMice KnockoutMutationWild typeCancerProto-Oncogene Proteins c-mdm2medicine.diseaseGenes p53HDAC13. Good healthGene Expression Regulation NeoplasticHistone Deacetylase InhibitorsPancreatic NeoplasmsDisease Models Animal030104 developmental biologyMutationCancer researchOncogene
researchProduct

Roles of TP53 in determining therapeutic sensitivity, growth, cellular senescence, invasion and metastasis.

2016

TP53 is a critical tumor suppressor gene that regulates cell cycle progression, apoptosis, cellular senescence and many other properties critical for control of normal cellular growth and death. Due to the pleiotropic effects that TP53 has on gene expression and cellular physiology, mutations at this tumor suppressor gene result in diverse physiological effects. T53 mutations are frequently detected in numerous cancers. The expression of TP53 can be induced by various agents used to treat cancer patients such as chemotherapeutic drugs and ionizing radiation. Radiation will induce Ataxia telangiectasia mutated (ATM) and other kinases that results in the phosphorylation and activation of TP53…

0301 basic medicineCancer Researchendocrine system diseasesMetastasimedicine.disease_causeMetastasisAntineoplastic AgentInvasionNeoplasmsTP53Neoplasm Metastasisbcl-2-Associated X ProteinAza CompoundProto-Oncogene ProteinApoptosis Regulatory ProteinbiologyCell CyclemiRMicroRNACell cycleCell biologyNeoplasm MetastasiGene Expression Regulation NeoplasticNutlin-3 chemosensitivityMdm2Molecular MedicineHumanSignal TransductionCyclin-Dependent Kinase Inhibitor p21Tumor suppressor genemiRsAntineoplastic AgentsCellular senescenceTP53; miRs; MDM2; Nutlin-3 chemosensitivity; Cellular senescence ; Invasion; Metastasis03 medical and health sciencesBcl-2-associated X proteinGeneticMDM2Proto-Oncogene ProteinsmicroRNAGeneticsmedicineHumansNeoplasm InvasivenessneoplasmsMolecular BiologyCell ProliferationNeoplasm InvasiveneAza CompoundsOncomirBridged Bicyclo Compounds HeterocyclicMicroRNAs030104 developmental biologyTumor progressionbiology.proteinNeoplasmTumor Suppressor Protein p53CarcinogenesisApoptosis Regulatory Proteins
researchProduct

Role of nitric oxide pathway in the conditioned rewarding effects of MDMA in mice.

2017

It is estimated that 2.1 million young adults used MDMA/Ecstasy in the last year in Europe. Vulnerable subjects can develop dependence after MDMA abuse but currently there does not exist an effective treatment for this disorder. The nitric oxide (NO) pathway seems to have an important role on the rewarding effects of different drugs and has been proposed as a new pharmacological treatment for psychostimulant addiction. In the present study, we intend to evaluate whether the blockade of the NO synthesis (NOS) interferes with the rewarding effects of MDMA in the conditioned preference place (CPP) paradigm in young adult male mice. Our results indicated that mice treated with 7-nitroindazole (…

0301 basic medicineHallucinogenMaleMDMA7-NitroindazoleIndazolesmedia_common.quotation_subjectN-Methyl-34-methylenedioxyamphetamineEcstasyConditioning ClassicalEnsayos clínicosPharmacologyNitric OxideNitric oxide03 medical and health sciencesBehavioral Neurosciencechemistry.chemical_compoundMice0302 clinical medicineRewardmental disordersConditioning PsychologicalmedicineAnimalsDrogasmedia_commonbiologyAddictionMDMABlockadeNitric oxide synthaseEfectos fisiológicos030104 developmental biologychemistrybiology.proteinHallucinogensConditioning OperantCentral Nervous System StimulantsNitric Oxide SynthasePsychologyEstupefacientepsychological phenomena and processes030217 neurology & neurosurgerymedicine.drugBehavioural brain research
researchProduct

Blockade of nitric oxide signalling promotes resilience to the effects of social defeat stress on the conditioned rewarding properties of MDMA in mice

2020

Abstract MDMA abuse continues being a serious problem in our society. Environmental factors, such as stress, increase the vulnerability of individuals to develop drug abuse and we have observed that exposure to social defeat (SD) stress alters the sensitivity of mice to the rewarding effects of MDMA in the conditioned place preference (CPP) paradigm. In the present study, we evaluated the role of the nitric oxide (NO) pathway in the effects of SD on the rewarding properties of MDMA. Three groups of mice were treated with an inhibitor of NO synthesis, 7-nitroindazole (0, 7.25 and 12.5 mg/kg), before each exposure to SD and place conditioning with MDMA (1.25 mg/kg) on PND 54, 56, 58, and 60. …

0301 basic medicineMaleCancer Researchmedicine.medical_specialty7-NitroindazoleIndazolesMDMAPhysiologyN-Methyl-34-methylenedioxyamphetamineClinical BiochemistryHippocampusMice Inbred StrainsStriatum030204 cardiovascular system & hematologyNitric OxideBiochemistrySocial defeat03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineSocial defeatInternal medicineConditioning Psychologicalmental disordersmedicineAnimalsPrefrontal cortex7-NitroindazoleSocial stressDose-Response Relationship Drugbusiness.industryMDMANitric oxideConditioned place preferenceConditioned place preference030104 developmental biologyEndocrinologychemistrybusinessStress Psychologicalpsychological phenomena and processesmedicine.drugSignal Transduction
researchProduct

Structure–Activity Relationship of Plesiomonas shigelloides Lipid A to the Production of TNF-α, IL-1β, and IL-6 by Human and Murine Macrophages

2017

Plesiomonas shigelloides is a Gram-negative bacterium that is associated with diarrheal disease in humans. Lipopolysaccharide (LPS) is the main surface antigen and virulence factor of this bacterium. The lipid A (LA) moiety of LPS is the main region recognized by target cells of immune system. Here, we evaluated the biological activities of P. shigelloides LA for their abilities to induce the productions of proinflammatory cytokines (TNF-α, IL-1β, and IL-6) by human and murine macrophages [THP-1 macrophages and immortalized murine bone marrow-derived macrophages (iBMDM)]. Four native P. shigelloides LA preparations differing in their phosphoethanolamine (PEtn) substitution, length, number, …

0301 basic medicinelcsh:Immunologic diseases. AllergyReceptor complexLipopolysaccharideImmunologymedicine.disease_causeVirulence factorProinflammatory cytokineLipid A03 medical and health scienceschemistry.chemical_compoundmedicineImmunology and AllergyEscherichia colilipid AOriginal ResearchbiologyChemistrylipopolysaccharidebiology.organism_classificationBMDMMolecular biologyIn vitro030104 developmental biologyPlesiomonas shigelloidesproinflammatory cytokinesPlesiomonasTHP-1lcsh:RC581-607Frontiers in Immunology
researchProduct

The Role of p53 Signaling in Colorectal Cancer.

2021

Simple Summary The transcription factor p53 is a crucial tumor suppressor that regulates diverse cellular responses to protect against cancer development. Deactivating p53 signaling either by altering p53 regulators or by p53 mutations occurs frequently in human colorectal carcinoma (CRC). Forty-three percent of CRCs harbor p53 mutations that reduce wild-type p53 tumor suppressor activity and often provide neo-morphic functions, which contribute to tumorigenesis. In this review, we summarize wild-type p53 signaling, how it can be deregulated in CRC, and the functional and phenotypical effects of p53 mutations. We also discuss current therapeutic strategies of targeting p53. Abstract The tra…

0301 basic medicinewild type p53Cancer ResearchDNA repairCellular differentiationcolorectal cancerReview03 medical and health sciences0302 clinical medicinemedicineTranscription factorRC254-282gain-of-functionbiologyCell growthmutant p53CancerNeoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseUbiquitin ligasep53 signaling030104 developmental biologyOncology030220 oncology & carcinogenesisCancer cellbiology.proteinCancer researchMdm2cancer therapyp53 pathwayCancers
researchProduct

MDM2 and CDKN1A gene polymorphisms and risk of Kaposi's sarcoma in African and Caucasian patients

2010

A single-nucleotide polymorphism in the MDM2 promoter (SNP309; rs2279744) causes elevated transcription of this major negative regulator of p53 in several cancer types. We investigated MDM2 SNP309 and CDKN1A (p21/Waf1/Cip1) codon 31 (rs1801270) polymorphisms in 86 cases of cutaneous Kaposi's sarcoma (KS) from African and Caucasian patients, and 210 healthy controls. A significant increase of the MDM2 SNP309 T/G genotype was observed among classic KS cases (odds ratio 2.38, 95% confidence interval 1.0-5.5). Frequencies of CDKN1A codon 31 genotypes were not significantly different between cases and controls. The results suggest that the MDM2 SNP309 G allele may act as a susceptibility gene fo…

AdultCyclin-Dependent Kinase Inhibitor p21MaleGenotypeHealth Toxicology and MutagenesisClinical BiochemistryBlack PeopleBiologyPolymorphism Single NucleotideBiochemistryWhite PeopleYoung AdultGene FrequencyRisk FactorsGenotypemedicineHumansGenetic Predisposition to DiseaseAlleleYoung adultSarcoma KaposiKaposi's sarcomaAllele frequencyAgedAged 80 and overProto-Oncogene Proteins c-mdm2Odds ratioMiddle Agedmedicine.diseaseConfidence intervalImmunologyCancer researchFemaleSarcomaTumor Suppressor Protein p53
researchProduct

Molecular analysis of the 9p21 locus and p53 genes in Ewing family tumors.

2001

The EWS-ETS rearrangements, and their respective fusion gene products, are specifically associated with histopathologically Ewing family tumors (EFT). These translocations are implicated in generating malignant transformation of EFT, but the presence of additional genetic alterations must be considered in the pathogenesis of such tumors. We analyzed 26 samples (biopsies and/or nude mice xenotransplants) collected from 19 patients with an EFT to determine whether molecular and cytogenetic alterations of the G(1)/S checkpoint genes are implicated in the pathogenesis of EFT. We found inactivating p53 mutations in three (16%) cases, which correlated with a loss of p21(WAF1/Cip1) expression and …

AdultCyclin-Dependent Kinase Inhibitor p21MaleMonosomyTumor suppressor geneAdolescentTransplantation HeterologousGene ExpressionChromosome 9Locus (genetics)Sarcoma EwingBiologymedicine.disease_causePathology and Forensic MedicineFusion geneMiceCyclinsProto-Oncogene ProteinsmedicineAnimalsHumansPoint MutationCyclin D1ChildMolecular BiologyGeneGene AmplificationChromosome MappingCyclin-Dependent Kinase 4Nuclear ProteinsProto-Oncogene Proteins c-mdm2Cell BiologyDNA Methylationmedicine.diseaseGenes p53Survival AnalysisCyclin-Dependent KinasesChromosome 17 (human)Child PreschoolCancer researchFemaleCarcinogenesisChromosomes Human Pair 9Gene DeletionNeoplasm TransplantationLaboratory investigation; a journal of technical methods and pathology
researchProduct

Genetic alterations and oxidative metabolism in sporadic colorectal tumors from a Spanish community

1997

Deletions of loci on chromosomes 5q, 17p, 18q, and 22q, together with the incidence of p53 mutations and amplification of the double minute-2 gene were investigated in the sporadic colorectal tumors of 44 patients from a Spanish community. Chromosome deletions were analyzed by means of loss of heterozygosity analysis using a restriction fragment length polymorphism assay. Allelic losses were also detected by polymerase chain reaction (PCR)-single-stranded conformation polymorphism (SSCP) analysis of a polymorphic site in intron 2 of the p53 gene. The percentages of genetic deletions on the screened chromosomes were 39.3% (5q), 58.3% (17p), 40.9% (18q), and 40% (22q). Mutations in p53 exons …

AdultGenetic MarkersMaleGenome instabilityHeterozygoteLipid PeroxidesCancer ResearchChromosomes Human Pair 22DNA Mutational AnalysisAdenocarcinomaBiologymedicine.disease_causeLoss of heterozygosityProto-Oncogene ProteinsGene duplicationmedicineHumansMolecular BiologyGenePolymorphism Single-Stranded ConformationalAgedSequence DeletionGene AmplificationDeoxyguanosineNuclear ProteinsProto-Oncogene Proteins c-mdm2Single-strand conformation polymorphismDNA NeoplasmMiddle AgedGenes p53GlutathioneMolecular biology8-Hydroxy-2'-DeoxyguanosineChromosomes Human Pair 1SpainGenetic markerChromosomes Human Pair 5FemaleRestriction fragment length polymorphismChromosomes Human Pair 18Colorectal NeoplasmsCarcinogenesisOxidation-Reduction
researchProduct