Search results for "unity"

showing 10 items of 3852 documents

R-Roscovitine (Seliciclib) prevents DNA damage-induced cyclin A1 upregulation and hinders non-homologous end-joining (NHEJ) DNA repair.

2010

Abstract Background CDK-inhibitors can diminish transcriptional levels of cell cycle-related cyclins through the inhibition of E2F family members and CDK7 and 9. Cyclin A1, an E2F-independent cyclin, is strongly upregulated under genotoxic conditions and functionally was shown to increase NHEJ activity. Cyclin A1 outcompetes with cyclin A2 for CDK2 binding, possibly redirecting its activity towards DNA repair. To see if we could therapeutically block this switch, we analyzed the effects of the CDK-inhibitor R-Roscovitine on the expression levels of cyclin A1 under genotoxic stress and observed subsequent DNA damage and repair mechanisms. Results We found that R-Roscovitine alone was unable …

Cancer ResearchDNA RepairDNA repairDNA damageSettore MED/06 - Oncologia MedicaCyclin DCyclin ACyclin BSettore BIO/11 - Biologia Molecolarelcsh:RC254-282RoscovitineProtein Kinase InhibitorsBIO/10 Biochimicaroscovitine doxorubicinbiologyResearchCyclin A1; Doxorubicin; Protein Kinase Inhibitors; Purines; Up-Regulation; DNA Damage; DNA Repair; Hydrogen-Ion Concentration; Cancer Research; Molecular Medicine; OncologyG2-M DNA damage checkpointHydrogen-Ion Concentrationlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensUp-RegulationOncologyDoxorubicinPurinesCancer researchbiology.proteinMolecular MedicineCyclin A1biological phenomena cell phenomena and immunityCyclin A1Cyclin A2DNA DamageMolecular cancer
researchProduct

Cleavage of CD95 by matrix metalloproteinase-7 induces apoptosis resistance in tumour cells

2004

The ability of tumour cells to resist apoptosis-inducing signals by cytotoxic T cells may decide the success or failure of tumour elimination. An important effector of apoptosis is the CD95/CD95 ligand system (APO-1/Fas) that mediates perforin-independent cytotoxic T-cell killing of tumour cells. We propose a new strategy by which tumour cells can resist CD95-induced apoptosis. We identified matrix metalloproteinase-7, MMP-7 (Martilysin), as the first physiologically relevant protease that can specifically cleave CD95. MMP-7 is of unique importance because it is produced by the tumour cells themselves at early stages of tumour development. Microsequencing of the positions in CD95 cleaved by…

Cancer ResearchEffectorApoptosishemic and immune systemschemical and pharmacologic phenomenaBiologyMatrix metalloproteinaseFas receptorCleavage (embryo)medicine.disease_causeCell biologyApoptosisMatrix Metalloproteinase 7hemic and lymphatic diseasesTumor Cells CulturedGeneticsExtracellularmedicineHumansCytotoxic T cellfas Receptorbiological phenomena cell phenomena and immunityCarcinogenesisMolecular BiologyOncogene
researchProduct

Cellular immune response to human renal-cell carcinomas: Definition of a common antigen recognized by HLA-A2-restricted cytotoxic T-Lymphocyte (CTL) …

1994

Cytotoxic T lymphocyte (CTL) clones directed against autologous renal-cell carcinoma (RCC) cell lines were generated by mixed lymphocyte/tumor-cell culture (MLTC) using peripheral blood lymphocytes (PBL). A CD8+, CD4- CTL clone MZ1257-CTL 5/30 with high cytolytic activity for the autologous tumor cell line MZ1257-RCC was established. No lysis of the autologous EBV-transformed B lymphocytes (EBV-B) or K562 cells was observed. A panel of HLA-A2-matched allogeneic RCC lines was recognized by CTL 5/30. Further specificity analysis showed a cross-reactivity with HLA-A2-matched allogeneic tumor cells of various origins, especially melanoma. CTL 5/30 was also cross-reactive with several HLA-A2-pos…

Cancer ResearchLymphocyteCross ReactionsBiologyKidneyImmune systemAntigenAntigens NeoplasmHLA-A2 AntigenTumor Cells CulturedmedicineHumansCytotoxic T cellCarcinoma Renal CellMelanomaImmunity CellularHistocompatibility Antigens Class IAntibodies MonoclonalT lymphocyteAntigens DifferentiationAutologous tumor cellKidney NeoplasmsCTL*medicine.anatomical_structureOncologyImmunologyLymphocyte Culture Test MixedClone (B-cell biology)T-Lymphocytes CytotoxicInternational Journal of Cancer
researchProduct

Recommendations from the iSBTc-SITC/FDA/NCI Workshop on Immunotherapy Biomarkers

2011

Abstract Purpose: To facilitate development of innovative immunotherapy approaches, especially for treatment concepts exploiting the potential benefits of personalized therapy, there is a need to develop and validate tools to identify patients who can benefit from immunotherapy. Despite substantial effort, we do not yet know which parameters of antitumor immunity to measure and which assays are optimal for those measurements. Experimental Design: The iSBTc-SITC (International Society for Biological Therapy of Cancer-Society for Immunotherapy of Cancer), FDA (Food and Drug Administration), and NCI (National Cancer Institute) partnered to address these issues for immunotherapy of cancer. Here…

Cancer ResearchPathologymedicine.medical_specialtyHealth Planning Guidelinesmedicine.medical_treatmentConsensus Development Conferences as TopicStandardized testImmune monitoringt-cell immunity cytokine flow-cytometry cancer vaccine consortium colony-stimulating factor b elispot assay phase-ii trial dendritic cells clinical-trials hiv vaccine harmonization guidelinesMedical OncologyArticleFood and drug administrationNeoplasmsmedicineBiomarkers TumorHumansMedical physicsPersonalized therapySocieties MedicalAntitumor immunitybusiness.industryQuality assessmentUnited States Food and Drug AdministrationCancerInternational AgenciesImmunotherapymedicine.diseaseNational Cancer Institute (U.S.)United StatesOncologyPractice Guidelines as TopicImmunotherapybusiness
researchProduct

Aurora-A Transcriptional Silencing and Vincristine Treatment Show a Synergistic Effect in Human Tumor Cells

2008

Aurora-A is a centrosome-associated serine/threonine kinase that is overexpressed in multiple types of human tumors. Primarily, Aurora-A functions in centrosome maturation and mitotic spindle assembly. Overexpression of Aurora-A induces centrosome amplification and G 2 /M cell cycle progression. Recently, it was observed that overexpression of Aurora-A renders cells resistant to cisplatin (CDDP)-, etoposide-, and paclitaxel-induced apoptosis.Our results indicate that already in initial stages of cancer progression Aurora-A overexpression could have a major role in inducing supernumerary centrosomes and aneuploidy, as shown by immunohistochemistry on tissue sections from various stages of hu…

Cancer ResearchPathologymedicine.medical_specialtyTranscription GeneticApoptosismacromolecular substancesProtein Serine-Threonine KinasesBiologyTransfectionPLK1Aurora KinasesRNA interferenceCell Line TumormedicineHumansGene silencingGene SilencingRNA Small InterferingMitotic catastropheCentrosomeCisplatinCarcinomaCell CycleDrug SynergismAuroraA/stk15centrosome amplificationAneuploidy CINGeneral MedicineCell cycleAneuploidyAntineoplastic Agents PhytogenicGene Expression Regulation NeoplasticSettore BIO/18 - Geneticaenzymes and coenzymes (carbohydrates)OncologyVincristineCentrosomeColonic Neoplasmsembryonic structuresCancer cellCancer researchbiological phenomena cell phenomena and immunityHeLa Cellsmedicine.drugOncology Research Featuring Preclinical and Clinical Cancer Therapeutics
researchProduct

Smac induces cytochrome c release and apoptosis independently from Bax/Bcl-xL in a strictly caspase-3-dependent manner in human carcinoma cells

2004

The mitochondrial apoptosis pathway mediates cell death through the release of various pro-apoptotic factors including cytochrome c and Smac, the second mitochondrial activator of caspases, into the cytosol. Smac was shown previously to inhibit IAP proteins and to facilitate initiation of the caspase cascade upon cytochrome c release. To investigate Smac function during apoptosis and to explore Smac as an experimental cancer therapeutic, we constructed an expression system based on a single adenoviral vector containing Smac under control of the Tet-off system supplied in cis. Conditional expression of Smac induced apoptosis in human HCT116 and DU145 carcinoma cells regardless of the loss of…

Cancer ResearchProgrammed cell deathbcl-X ProteinApoptosisBreast NeoplasmsBcl-xLCaspase 3Cysteine Proteinase InhibitorsAdenoviridaeMitochondrial ProteinsBcl-2-associated X proteinProto-Oncogene ProteinsTumor Cells CulturedGeneticsHumansMolecular BiologyCaspasebcl-2-Associated X ProteinCaspase-9biologyCaspase 3Cytochrome cCarcinomaIntracellular Signaling Peptides and ProteinsCytochromes cCaspase InhibitorsCaspase 9Cell biologyEnzyme ActivationProto-Oncogene Proteins c-bcl-2ApoptosisCaspasesMutationbiology.proteinCancer researchbiological phenomena cell phenomena and immunityApoptosis Regulatory ProteinsCarrier ProteinsOligopeptidesProtein Processing Post-TranslationalOncogene
researchProduct

Ub surprised: viral ovarian tumor domain proteases remove ubiquitin and ISG15 conjugates.

2007

Ubiquitin (Ub) and interferon stimulated gene product 15 (ISG15) reversibly conjugate to proteins via a conserved LRLRGG C-terminal motif, mediating important innate antiviral responses. The ovarian tumor (OTU) domain represents a superfamily of predicted proteases found in eukaryotic, bacterial and viral proteins, some of which have Ub-deconjugating activity. We show that the OTU domain-containing proteases of nairoviruses and arteriviruses hydrolyze Ub and ISG15 from cellular target proteins. This broad activity contrasts with the target specificity of known mammalian OTU domain-containing proteins. The biological significance of this activity of viral OTU domain-containing proteases was …

Cancer ResearchProteasesCellPeptideBiologyMicrobiologyArticleOvarian tumorViral ProteinsUbiquitinImmunology and Microbiology(all)VirologymedicineHumansMolecular BiologyUbiquitinschemistry.chemical_classificationVirologyISG15Immunity InnateCell biologyNeoplasm ProteinsProtein Structure Tertiarymedicine.anatomical_structureViral replicationchemistrybiology.proteinCytokinesParasitologyConjugatePeptide HydrolasesSignal TransductionCell hostmicrobe
researchProduct

Toll-like receptors: Expression and involvement in Multiple Myeloma

2010

Multiple Myeloma (MM) cells express and respond to a broad range of TLRs. Accumulating evidences suggest that TLRs act as double-edged sword in MM biology. Indeed, TLR9 or TLR3 ligands could enhance immunity against MM cells or directly induce cell apoptosis, whereas various TLR agonists could induce MM survival, proliferation, and immune escape. This review is focused on the heterogeneous expression and function of TLRs in MM and on the potential implication of TLR ligands of infectious or endogenous origin in MM emergence, resistance, or progression.

Cancer ResearchTLR9ApoptosisEndogenyHematologyBiologyLigandsmedicine.diseaseToll-Like Receptor 3Cell biologyGene Expression Regulation NeoplasticImmune systemOncologyApoptosisImmunityToll-Like Receptor 9TLR3medicineAnimalsHumansTumor EscapeMultiple MyelomaReceptorMultiple myelomaLeukemia Research
researchProduct

pRb2/p130-E2F4/5-HDAC1-SUV39H1-p300 and pRb2/p130-E2F4/5-HDAC1-SUV39H1-DNMT1 multimolecular complexes mediate the transcription of estrogen receptor-…

2003

The estrogen receptor-alpha (ER) plays a crucial role in normal breast development and is also linked to development and progression of mammary carcinoma. The transcriptional repression of ER-alpha gene in breast cancer is an area of active investigation with potential clinical significance. However, the molecular mechanisms that regulate the ER-alpha gene expression are not fully understood. Here we show a new molecular mechanism of ER-alpha gene inactivation mediated by pRb2/p130 in ER-negative breast cancer cells. We investigated in vivo occupancy of ER-alpha promoter by pRb2/p130-E2F4/5-HDAC1-SUV39 H1-p300 and pRb2/p130-E2F4/5-HDAC1-SUV39H1-DNMT1 complexes, and provided a link between p…

Cancer ResearchTranscription GeneticEstrogen receptorHistone Deacetylase 1HistonesTumor Cells CulturedDNA (Cytosine-5-)-MethyltransferasesReceptorPromoter Regions GeneticE2F4Nuclear ProteinsAcetylationChromatinDNA-Binding ProteinsGene Expression Regulation NeoplasticReceptors Estrogenembryonic structuresDNA methylationFemalepRb2/p130; chromatin-modifying enzymes; estrogen receptor-alpha; breast carcinomabiological phenomena cell phenomena and immunityDNA (Cytosine-5-)-Methyltransferase 1medicine.medical_specialtyanimal structuresmedicine.drug_classMacromolecular SubstancesBreast NeoplasmsE2F4 Transcription FactorBiologyHistone DeacetylasesBreast cancerInternal medicineGeneticsmedicineEstrogen Receptor betaHumansMolecular BiologyEstrogen receptor betaE2F5 Transcription FactorRetinoblastoma-Like Protein p130Estrogen Receptor alphaProteinsMethyltransferasesDNA Methylationmedicine.diseasePhosphoproteinsRepressor Proteinsenzymes and coenzymes (carbohydrates)EndocrinologyEstrogenCancer researchTrans-ActivatorsEstrogen receptor alphaTranscription FactorsOncogene
researchProduct

AURKA (aurora kinase A)

2011

Review on AURKA (aurora kinase A), with data on DNA, on the protein encoded, and where the gene is implicated.

Cancer Researchmacromolecular substancesHematologyBiologyCell biologySettore BIO/18 - Geneticaenzymes and coenzymes (carbohydrates)chemistry.chemical_compoundOncologychemistryembryonic structuresGeneticsAurora Kinase Abiological phenomena cell phenomena and immunityAURK-AGeneDNAAtlas of Genetics and Cytogenetics in Oncology and Haematology
researchProduct