Search results for "tumor suppressor gene"

showing 10 items of 98 documents

Epigenetic Alterations Upstream and Downstream of p53 Signaling in Colorectal Carcinoma

2021

Simple Summary Colorectal cancer (CRC) belongs to the most common cancer types. It is well known that half of all CRC possess missense mutations in the TP53 tumor suppressor gene. However, the entire signaling cascade upstream and downstream of the p53 protein may also contribute to CRC development, if relevant players in this signaling cascade lost their function. Besides p53 loss-of-function by mutations, epigenetic changes (DNA methylation, post translational modifications of histones, micro-RNAs) play a vital role in CRC development. In the present review, we concentrated on the epigenetic modifications related to the entire p53 signal transduction cascade upstream and downstream of p53…

Cancer ResearchTumor suppressor genetumor suppressorUpstream and downstream (transduction)Reviewmedicine.disease_causeoncogenemicroRNAmedicineEpigeneticsneoplasmsRC254-282acetylationbiologymicro-RNANeoplasms. Tumors. Oncology. Including cancer and carcinogensMethylationdigestive system diseasesHistoneOncologyDNA methylationCancer researchbiology.proteinmethylationCarcinogenesiscarcinogenesissignal transductionCancers
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Tracheal development and the von Hippel-Lindau tumor suppressor homolog in Drosophila.

2000

von Hippel-Lindau disease is a hereditary cancer syndrome. Mutations in the VHL tumor suppressor gene predispose individuals to highly vascularized tumors. However, VHL-deficient mice die in utero due to a lack of vascularization in the placenta. To resolve the contradiction, we cloned the Drosophila VHL homologue (d-VHL) and studied its function. It showed an overall 50% similarity to the human counterpart and 76% similarity in the crucial functional domain: the elongin C binding site. The putative d-VHL protein can bind Drosophila elongin C in vitro. During embryogenesis, d-VHL is expressed in the developing tracheal regions where tube outgrowth no longer occurs. Reduced d-VHL activity (u…

Cancer Researchendocrine system diseasesTumor suppressor geneUbiquitin-Protein LigasesMolecular Sequence Dataurologic and male genital diseasesTube fusionLigasesRNA interferenceVon Hippel–Lindau tumor suppressorGeneticsmedicineAnimalsHumansGenes Tumor SuppressorAmino Acid SequenceVon Hippel–Lindau diseaseCloning MolecularneoplasmsMolecular BiologyGeneticsbiologyTumor Suppressor ProteinsProteinsCell migrationEmbryomedicine.diseasePhenotypefemale genital diseases and pregnancy complicationsCell biologyTracheaPhenotypeVon Hippel-Lindau Tumor Suppressor Proteinbiology.proteinDrosophilaOncogene
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Experimental evolution of an oncolytic vesicular stomatitis virus with increased selectivity for p53-deficient cells

2014

Experimental evolution has been used for various biotechnological applications including protein and microbial cell engineering, but less commonly in the field of oncolytic virotherapy. Here, we sought to adapt a rapidly evolving RNA virus to cells deficient for the tumor suppressor gene p53, a hallmark of cancer cells. To achieve this goal, we established four independent evolution lines of the vesicular stomatitis virus (VSV) in p53-knockout mouse embryonic fibroblasts (p53-/- MEFs) under conditions favoring the action of natural selection. We found that some evolved viruses showed increased fitness and cytotoxicity in p53-/- cells but not in isogenic p53+/+ cells, indicating gene-specifi…

Cancer TreatmentVirus OncolíticosProtein EngineeringMiceMedicine and Health SciencesMacromolecular EngineeringMice KnockoutOncolytic VirotherapyMultidisciplinaryQProteína p53 Supresora de TumorRNeoplasias de la Mama3. Good healthOncolytic VirusesOncologyVesicular stomatitis virusColonic NeoplasmsMedicineFemaleVesicular StomatitisResearch ArticleBiotechnologyDirected EvolutionEvolutionary ProcessesTumor suppressor geneScienceBioengineeringBreast NeoplasmsBiologyMicrobiologyViral EvolutionVirusVesicular StomatitisVirologyCell Line TumorGeneticsAnimalsHumansEvolutionary BiologyNeoplasias del ColonBiology and Life SciencesRNA virusVesiculovirusbiology.organism_classificationVirologyOrganismal EvolutionOncolytic virusAnimal Models of InfectionArtificial SelectionSynthetic BioengineeringViruses and CancerCell cultureMicrobial EvolutionCancer cellCancer researchDirected Molecular EvolutionTumor Suppressor Protein p53
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Delayed ageing through damage protection by the Arf/p53 pathway.

2007

The tumour-suppressor pathway formed by the alternative reading frame protein of the Cdkn2a locus (Arf) and by p53 (also called Trp53) plays a central part in the detection and elimination of cellular damage, and this constitutes the basis of its potent cancer protection activity. Similar to cancer, ageing also results from the accumulation of damage and, therefore, we have reasoned that Arf/p53 could have anti-ageing activity by alleviating the load of age-associated damage. Here we show that genetically manipulated mice with increased, but otherwise normally regulated, levels of Arf and p53 present strong cancer resistance and have decreased levels of ageing-associated damage. These obser…

Cell signalingAgingTime FactorsTumor suppressor geneLongevityBiologymedicine.disease_causeAntioxidantsTranscriptomeMiceCDKN2ANeoplasmsmedicineAnimalsCells CulturedCyclin-Dependent Kinase Inhibitor p16MultidisciplinaryCell cycleFibroblastsCell biologyOxidative StressAgeingDisease SusceptibilitySignal transductionTumor Suppressor Protein p53Oxidative stressNature
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Mind-body medicine: stress and its impact on overall health and longevity.

2005

During evolution, DNA viruses have captured a broad array of cellular genes involved in immune recognition and growth control that are nonessential for viral replication. The encoded virokines and viroceptors may act as mimetics or antagonists of their cellular homologues, altering signal transduction and cell communication towards survival of virus-infected cells. Human herpesvirus type 8 (HHV8) is the most recently identified human oncogenic herpesvirus. It is associated with Kaposi's sarcoma and lymphoproliferative diseases, such as pleural effusion lymphomas and multicentric Castleman's disease. HHV8 has captured a unique number of cellular regulatory genes, which redirect gene expressi…

Cell signalingTumor suppressor genemedicine.medical_treatmentLongevityBiologyVirokineGeneral Biochemistry Genetics and Molecular BiologyMind-Body Relations MetaphysicalParacrine signallingHistory and Philosophy of ScienceStress PhysiologicalNeoplasmsmedicineHumansDiseaseAutocrine signallingGeneral Neurosciencevirus diseasesBrainPsychoneuroimmunologyCytokineViral replicationHealthImmunologyCancer researchSignal transductionAnnals of the New York Academy of Sciences
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Activated kRas protects colon cancer cells from cucurbitacin-induced apoptosis: The role of p53 and p21

2008

Cucurbitacins have been shown to inhibit proliferation in a variety of cancer cell lines. The aim of this study was to determine their biological activity in colon cancer cell lines that do not harbor activated STAT3, the key target of cucurbitacin. In order to establish the role of activated kRas in the responsiveness of cells to cucurbitacins, we performed experiments in isogenic colon cancer cell lines, HCT116 and Hke-3, which differ only by the presence of an activated kRas allele. We compared the activity of 23, 24-dihydrocucurbitacin B (DHCB) and cucurbitacin R (CCR), two cucurbitacins that we recently isolated, with cucurbitacin I (CCI), a cucurbitacin with established antitumorigeni…

Cyclin-Dependent Kinase Inhibitor p21Programmed cell deathTumor suppressor geneAntineoplastic AgentsApoptosisBiologymedicine.disease_causeBiochemistryArticleProto-Oncogene Proteins p21(ras)CucurbitacinsCell Line TumorProto-Oncogene ProteinsmedicineHumansCell ProliferationPharmacologyCell growthCucurbitacinTriterpenesdigestive system diseasesCell cultureApoptosisColonic Neoplasmsras ProteinsCancer researchKRASTumor Suppressor Protein p53Biochemical Pharmacology
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A p16INK4a-insensitive CDK4 mutant targeted by cytolytic T lymphocytes in a human melanoma.

1995

A mutated cyclin-dependent kinase 4 (CDK4) was identified as a tumor-specific antigen recognized by HLA-A2. 1-restricted autologous cytolytic T lymphocytes (CTLs) in a human melanoma. The mutated CDK4 allele was present in autologous cultured melanoma cells and metastasis tissue, but not in the patient's lymphocytes. The mutation, an arginine-to-cysteine exchange at residue 24, was part of the CDK4 peptide recognized by CTLs and prevented binding of the CDK4 inhibitor p16INK4a, but not of p21 or of p27KIP1. The same mutation was found in one additional melanoma among 28 melanomas analyzed. These results suggest that mutation of CDK4 can create a tumor-specific antigen and can disrupt the ce…

Cyclin-Dependent Kinase Inhibitor p21Tumor suppressor geneMutantMolecular Sequence DataCell Cycle ProteinsBiologyProtein Serine-Threonine Kinasesmedicine.disease_causeTransfectionPolymerase Chain ReactionMetastasisCell LineAntigenCyclinsProto-Oncogene ProteinsHLA-A2 AntigenmedicineTumor Cells CulturedAnimalsHumansPoint MutationAmino Acid SequenceCloning MolecularneoplasmsMelanomaCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p15MutationMultidisciplinaryintegumentary systemBase SequenceMelanomaTumor Suppressor ProteinsCyclin-Dependent Kinase 4Cell cyclemedicine.diseaseCyclin-Dependent KinasesCytolysisCancer researchCarrier ProteinsMicrotubule-Associated ProteinsCyclin-Dependent Kinase Inhibitor p27T-Lymphocytes CytotoxicScience (New York, N.Y.)
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Prognostic Value of p53, p21/WAF1, Bcl-2, Bax, Bak and Ki-67 Immunoreactivity in pT1 G3 Urothelial Bladder Carcinomas

2001

pT1 G3 bladder carcinomas are heterogeneous with respect to tumor recurrence and progression. Whereas some urologists treat these carcinomas by repeated transurethral resections often followed by intravesical chemotherapy or BCG instillation, others recommend cystectomy after tumor recurrence or early cystectomy after the initial diagnosis. Our goal was to determine the prognostic value of p53, p21/WAF1, Bcl-2, Bax, Bak, and Ki-67 immunoreactivity in these tumors. There were 30 patients with a new histopathological diagnosis of pT1 G3 urothelial carcinoma based on a transurethral resection specimen. Representative sections of these specimens were examined for the above markers. All patients…

Cyclin-Dependent Kinase Inhibitor p21medicine.medical_specialtyPathologyTime FactorsTumor suppressor genemedicine.medical_treatmentBcl 2 baxUrologyDisease-Free SurvivalCystectomyPredictive Value of TestsCyclinsProto-Oncogene ProteinsBiomarkers TumormedicineHumansNeoplasm InvasivenessRetrospective Studiesbcl-2-Associated X ProteinCarcinoma Transitional CellUrinary bladderBladder cancerbiologyMembrane ProteinsGeneral MedicinePrognosismedicine.diseaseImmunohistochemistrySurvival RateKi-67 Antigenbcl-2 Homologous Antagonist-Killer Proteinmedicine.anatomical_structureTransitional cell carcinomaProto-Oncogene Proteins c-bcl-2Urinary Bladder NeoplasmsTumor progressionKi-67biology.proteinTumor Suppressor Protein p53Follow-Up StudiesTumor Biology
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A loop involving NRF2, miR‐29b‐1‐5p and AKT, regulates cell fate of MDA‐MB‐231 triple‐negative breast cancer cells

2019

The present study shows that nuclear factor erythroid 2-related factor 2 (NRF2) and miR-29b-1-5p are two opposite forces which could regulate the fate of MDA-MB-231 cells, the most studied triple-negative breast cancer (TNBC) cell line. We show that NRF2 activation stimulates cell growth and markedly reduces reactive oxygen species (ROS) generation, whereas miR-29b-1-5p overexpression increases ROS generation and reduces cell proliferation. Moreover, NRF2 downregulates miR-29b-1-5p expression, whereas miR-29b-1-5p overexpression decreases p-AKT and p-NRF2. Furthermore, miR-29b-1-5p overexpression induces both inhibition of DNA N-methyltransferases (DNMT1, DNMT3A, and DNMT3B) expression and …

DNA (Cytosine-5-)-Methyltransferase 10301 basic medicineNF-E2-Related Factor 2PhysiologyClinical BiochemistryTriple Negative Breast NeoplasmsAKT DNMTs miR‐29b‐1‐5p NRF2 parthenolide tumor suppressor genesCell fate determinationenvironment and public healthDNA Methyltransferase 3A03 medical and health scienceschemistry.chemical_compound0302 clinical medicineSettore BIO/10 - BiochimicaCell Line TumorCyclin D2HumansParthenolideDNA (Cytosine-5-)-MethyltransferasesProtein kinase BTriple-negative breast cancerCell Proliferationchemistry.chemical_classificationReactive oxygen speciesCell growthTumor Suppressor ProteinsCell BiologyDNA Methylationrespiratory systemCell biologyGene Expression Regulation NeoplasticMicroRNAs030104 developmental biologychemistryCell culture030220 oncology & carcinogenesisDNMT1FemaleReactive Oxygen SpeciesProto-Oncogene Proteins c-aktSesquiterpenesSignal TransductionJournal of Cellular Physiology
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Tumor suppression inDrosophila is causally related to the function of thelethal(2)tumorous imaginal discs gene, adnaJ homolog

1995

The Drosophila melanogaster tumor suppressor gene lethal(2)tumorous imaginal discs (l(2)tid) causes in homozygotes malignant growth of cells of the imaginal discs and the death of the mutant larvae at the time of puparium formation. We describe the molecular cloning of the l(2)tid+ gene and its temporal expression pattern in the wild-type and mutant alleles. Germ line rescue of the tumor phenotype was achieved with a 7.0 kb Hindlll-fragment derived from the polytene chromosome band 59F5. The l(2)tid+ gene spans approximately 2.5 kb of genomic DNA. The protein coding region, 1,696 bps long, is divided by an intron into two exons. The predicted Tid56 protein contains 518 amino acids and posse…

DNA ComplementarySaccharomyces cerevisiae ProteinsTumor suppressor geneMolecular Sequence DataMutantGenes InsectSaccharomyces cerevisiaeAnimals Genetically ModifiedFungal ProteinsMitochondrial ProteinsSpecies SpecificityEscherichia coliGeneticsAnimalsDrosophila ProteinsHumansGenes Tumor SuppressorAmino Acid SequenceCloning MolecularGeneAllelesHeat-Shock ProteinsPolytene chromosome bandBase SequenceSequence Homology Amino AcidbiologyEscherichia coli ProteinsPupaChromosome MappingExonsNeoplasms ExperimentalCell BiologyHSP40 Heat-Shock Proteinsbiology.organism_classificationMolecular biologyImaginal discDrosophila melanogasterLarvaDNAJA2Drosophila melanogasterSequence AlignmentDrosophila ProteinDevelopmental BiologyDevelopmental Genetics
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