Search results for "MESH: Antineoplastic Agents"

showing 7 items of 7 documents

[Appropriate cytotoxic drug usages in solid tumors: conformity to official labelling and level of scientific evidence]

2006

International audience; The definition of appropriate use of drugs is questioned in oncology. Daily therapeutic practices were compared to official labelling and to published scientific data in this retrospective study. It was carried out in two respective specialised centers, from January to September 2004. All chemotherapies administered for adult solid tumours and including one of the eleven studied drugs were evaluated. The analysis of use was performed by drug : conformity to the validated labelling and level of scientific evidence (at the period study). The study included 1,561 drug uses in 1,211 patients. The overall rate of conformity to official labelling was 81.7 % (67.1 % of stri…

AdultMaleAdolescentMESH : Retrospective StudiesMESH : MaleMESH: Drug LabelingMESH : AgedAntineoplastic Agents[SDV.CAN]Life Sciences [q-bio]/Cancer[ SDV.CAN ] Life Sciences [q-bio]/CancerMESH : BenchmarkingMESH : Drug LabelingMESH: Aged 80 and overMESH: Practice Guidelines as TopicMESH: Benchmarking[SDV.CAN] Life Sciences [q-bio]/CancerNeoplasmsMESH : AdolescentHumansMESH: NeoplasmsMESH : Middle AgedMESH : FemaleMESH : Aged 80 and overAgedDrug LabelingRetrospective StudiesAged 80 and overMESH: AdolescentMESH: AgedMESH: HumansMESH: Middle AgedMESH : HumansMESH: AdultMESH: Retrospective StudiesMiddle AgedMESH : AdultMESH : NeoplasmsMESH: MaleBenchmarkingMESH : Practice Guidelines as TopicMESH : Antineoplastic AgentsPractice Guidelines as TopicMESH: Antineoplastic AgentsFemaleMESH: Female
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TRAIL in cancer therapy: present and future challenges.

2007

International audience; Since its identification in 1995, TNF-related apoptosis-inducing ligand (TRAIL) has sparked growing interest in oncology due to its reported ability to selectively trigger cancer cell death. In contrast to other members of the TNF superfamily, TRAIL administration in vivo is safe. The relative absence of toxic side effects of this naturally occurring cytokine, in addition to its antitumoural properties, has led to its preclinical evaluation. However, despite intensive investigations, little is known in regards to the mechanisms underlying TRAIL selectivity or efficiency. An appropriate understanding of its physiological relevance, and of the mechanisms controlling ca…

MESH: Signal Transductionmedicine.medical_treatmentClinical BiochemistryApoptosisTRAILTNF-Related Apoptosis-Inducing LigandBioinformaticsTNF-Related Apoptosis-Inducing LigandMESH : TNF-Related Apoptosis-Inducing Ligand0302 clinical medicineDrug Delivery SystemsNeoplasmsDrug DiscoveryMESH: AnimalsMESH: Neoplasms0303 health sciencesTnf superfamily3. Good healthMESH : Antineoplastic AgentsCytokine030220 oncology & carcinogenesisMolecular MedicineMESH : Drug Delivery SystemsTRAIL-Receptors.Signal transductionMESH: TNF-Related Apoptosis-Inducing LigandSignal TransductionMESH: ForecastingProgrammed cell deathMESH: Drug Delivery SystemsCancer therapyAntineoplastic AgentsArticleresistance03 medical and health sciencesmedicine[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyAnimalsHumanscancer[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH : ForecastingTRAIL-receptor agonistic antibodies[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biology030304 developmental biologyPharmacologyMESH : Signal TransductionMESH: Humansbusiness.industryMESH: ApoptosisMESH : HumansCancermedicine.diseaseMESH : NeoplasmsCancer cellImmunologyMESH: Antineoplastic AgentsMESH : AnimalsbusinessTRAIL-ReceptorsMESH : ApoptosisForecasting
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Bax-derived membrane-active peptides act as potent and direct inducers of apoptosis in cancer cells.

2011

SUMMARYAlthough many cancer cells are primed for apoptosis, they usually develop resistance to cell death at multiple levels. Permeabilization of the outer mitochondrial membrane, which is mediated by proapoptotic Bcl-2 family members like Bax, is considered as a point-of-no-return for initiating apoptotic cell death. This crucial role has placed Bcl-2 family proteins as recurrent targets for anticancer drug development. Here, we propose and demonstrate a new concept based on using minimal active version of Bax to induce cell death independently of endogenous Bcl-2 proteins. We show that membrane-active segments of Bax can directly induce the release of mitochondria-residing apoptogenic fac…

ApoptosisMitochondrionMiceMESH: Protein Structure Tertiary0302 clinical medicineNeoplasmsgeneticsMESH: AnimalsMESH: Neoplasmsbcl-2-Associated X Protein0303 health sciencesbiologyMESH: PeptidesCytochrome capoptosisCytochromes cMESH: Cytochromes cproapoptotic BaxCell biologyMitochondriadrug therapymitochondria030220 oncology & carcinogenesisBacterial outer membraneProgrammed cell deathMESH: Cell Line TumorMESH: MitochondriaAntineoplastic Agents[SDV.CAN]Life Sciences [q-bio]/Cancerpore-forming peptideschemistryArticle03 medical and health sciencesBcl-2-associated X proteinBcl-2 familyCell Line TumorAnimalsHumansMESH: bcl-2-Associated X ProteinMESH: Mice030304 developmental biologyMESH: HumansMESH: ApoptosisBcl-2 familyCell BiologyProtein Structure Tertiaryanticancer agentantivascular therapyApoptosisdrug effectsCancer cellbiology.proteinMESH: Antineoplastic AgentspharmacologyphysiopathologyPeptidesmetabolism
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Dacarbazine-mediated upregulation of NKG2D ligands on tumor cells activates NK and CD8 T cells and restrains melanoma growth.

2013

International audience; Dacarbazine (DTIC) is a cytotoxic drug widely used for melanoma treatment. However, the putative contribution of anticancer immune responses in the efficacy of DTIC has not been evaluated. By testing how DTIC affects host immune responses to cancer in a mouse model of melanoma, we unexpectedly found that both natural killer (NK) and CD8(+) T cells were indispensable for DTIC therapeutic effect. Although DTIC did not directly affect immune cells, it triggered the upregulation of NKG2D ligands on tumor cells, leading to NK cell activation and IFNγ secretion in mice and humans. NK cell-derived IFNγ subsequently favored upregulation of major histocompatibility complex cl…

Skin NeoplasmsMelanoma ExperimentalCD8-Positive T-LymphocytesPharmacologyMESH: Antineoplastic Agents AlkylatingLigandsBiochemistryMiceInterleukin 210302 clinical medicineMESH: Up-RegulationMESH: LigandsCytotoxic T cell[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyMESH: AnimalsMESH : Up-RegulationMESH : LigandsMESH : Melanoma ExperimentalMelanomaMESH : Mice NudeMESH : CD8-Positive T-LymphocytesMESH: CD8-Positive T-LymphocytesUp-Regulation3. Good healthDacarbazineKiller Cells NaturalMESH: Melanoma ExperimentalNK Cell Lectin-Like Receptor Subfamily K030220 oncology & carcinogenesisMESH: NK Cell Lectin-Like Receptor Subfamily K[SDV.IMM]Life Sciences [q-bio]/ImmunologyMESH : Killer Cells Naturalmedicine.drugMESH: Killer Cells NaturalMESH: Cell Line Tumor[SDV.IMM] Life Sciences [q-bio]/ImmunologyMESH: Interferon-gammaDacarbazineMESH : Antineoplastic Agents AlkylatingMice NudeMESH : Mice Inbred C57BLDermatologyBiologyMajor histocompatibility complexMESH: DacarbazineInterferon-gamma03 medical and health sciencesImmune systemDownregulation and upregulationMESH: Mice Inbred C57BLCell Line TumorMESH : MicemedicineMESH : NK Cell Lectin-Like Receptor Subfamily KMESH: Mice NudeAnimalsHumansMESH : DacarbazineAntineoplastic Agents AlkylatingMolecular BiologyMESH: MiceMESH : Interferon-gammaMESH: HumansMESH : Cell Line TumorMESH: Skin NeoplasmsMESH : Skin NeoplasmsMESH : HumansCell Biologymedicine.diseaseMESH : Disease Models AnimalMice Inbred C57BLDisease Models Animalbiology.proteinMESH : AnimalsMESH: Disease Models AnimalCD8030215 immunology
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Wee1 inhibition potentiates Wip1-dependent p53-negative tumor cell death during chemotherapy

2016

AbstractInactivation of p53 found in more than half of human cancers is often associated with increased tumor resistance to anti-cancer therapy. We have previously shown that overexpression of the phosphatase Wip1 in p53-negative tumors sensitizes them to chemotherapeutic agents, while protecting normal tissues from the side effects of anti-cancer treatment. In this study, we decided to search for kinases that prevent Wip1-mediated sensitization of cancer cells, thereby interfering with efficacy of genotoxic anti-cancer drugs. To this end, we performed a flow cytometry-based screening in order to identify kinases that regulated the levels of γH2AX, which were used as readout. Another criter…

Wip1ApoptosisCell Cycle ProteinsPharmacologyMESH: G2 Phase Cell Cycle CheckpointsHistonesMESH : PhosphorylationMiceMESH : Cell Cycle ProteinsMESH: AnimalsMESH: Tumor Suppressor Protein p53MESH: HistonesKinaseTp53 mutationsMESH : Mice Transgenic3. Good healthProtein Phosphatase 2CSurvival RateMESH : Antineoplastic AgentsH2ax phosphorylationP53 activationMESH: Protein Phosphatase 2CRNA InterferenceMESH : Colorectal NeoplasmsMESH : Carrier ProteinsHistone H2axMESH: MitochondriaImmunologyHuman fibroblastsMESH: Carrier ProteinsAntineoplastic AgentsMESH: Protein-Tyrosine KinasesMESH: Protein-Serine-Threonine KinasesMESH : Cisplatin03 medical and health sciencesMESH: Cell Cycle ProteinsGenotoxic stressMESH : Protein-Tyrosine KinasesHumansMESH : HistonesAnticancer TherapyMESH: DNA DamageCisplatinMESH: HumansMESH: Phosphorylation[ SDV.BC ] Life Sciences [q-bio]/Cellular BiologyMESH : HumansMESH : Nuclear Proteins030104 developmental biologyCancer cellMESH: Antineoplastic AgentsCisplatinCarrier ProteinsMESH: Nuclear ProteinsMESH : ApoptosisDna-damage response0301 basic medicineCancer ResearchMESH: Caspase 3MESH : Caspase 3PhosphorylationCytotoxicityMESH : DNA DamageSensitizationmedicine.diagnostic_testCaspase 3Nuclear ProteinsProtein-Tyrosine KinasesMESH : Survival RateMitochondriaG2 Phase Cell Cycle CheckpointsWee1medicine.anatomical_structureMESH : Protein Phosphatase 2COriginal ArticleMESH : MitochondriaColorectal Neoplasmsmedicine.drugMESH : Protein-Serine-Threonine KinasesMESH: Cell Line TumorMESH: Survival RateMESH: Mice TransgenicMESH: RNA InterferencePhosphataseMice Transgenic[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologyProtein Serine-Threonine KinasesFlow cytometryCellular and Molecular NeuroscienceCell Line TumorMESH : MicemedicineAnimalsMESH: MiceMESH : Cell Line TumorMESH: ApoptosisCell BiologyMESH : Tumor Suppressor Protein p53MESH: CisplatinCancer researchbiology.proteinMESH : AnimalsMESH : G2 Phase Cell Cycle CheckpointsMESH : RNA InterferenceTumor Suppressor Protein p53MESH: Colorectal NeoplasmsDNA DamageCell Death & Disease
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Intra-arterial idarubicin_lipiodol without embolization can provide prolonged complete response in hepatocellular carcinoma: A case report.

2020

International audience; Hepatocellular carcinoma is the fourth leading cause of cancer death. For unresectable intermediate-stage hepatocellular carcinoma, the standard treatment is transarterial chemoembolization. To date, the overall survival at three years remains low, and there is currently no consensus about the best anticancer agent and optimal treatment regimen. We report the case of a hepatocellular carcinoma patient with a vascular contraindication to embolization who achieved a complete response after four intra-arterial infusions of idarubicin emulsified with lipiodol. The patient maintained his response over a three-year period without any hepatocellular carcinoma treatment, dem…

MaleHepatocellular carcinoma[SDV.IB.IMA]Life Sciences [q-bio]/Bioengineering/Imagingmedicine.medical_treatmentGastroenterologyEthiodized Oil0302 clinical medicineMESH: Infusions Intra-ArterialMESH: Liver NeoplasmsPharmacology (medical)EmbolizationMESH: Carcinoma HepatocellularComplete responseMESH: Treatment OutcomeMESH: AgedStandard treatmentLiver Neoplasms[SDV.SP]Life Sciences [q-bio]/Pharmaceutical sciences3. Good healthTreatment OutcomeOncology030220 oncology & carcinogenesisHepatocellular carcinomaLipiodol030211 gastroenterology & hepatologymedicine.drugmedicine.medical_specialtyIntra-arterial therapyCarcinoma HepatocellularAntineoplastic Agents[SDV.CAN]Life Sciences [q-bio]/Cancer03 medical and health sciencesMESH: Ethiodized OilInternal medicinemedicineHumansInfusions Intra-ArterialIdarubicinContraindicationAgedMESH: Humansbusiness.industryMESH: Idarubicinmedicine.diseasedigestive system diseasesMESH: MaleRegimenMESH: Antineoplastic AgentsbusinessIdarubicin
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Inhibitory effects oftrans-resveratrol analogs molecules on the proliferation and the cell cycle progression of human colon tumoral cells

2008

International audience; Resveratrol may function as a cancer chemopreventive agent. However, few data are available on the antitumoral activities of its dimer, epsilon-viniferin, also present in human diet. So, the effects of resveratrol, epsilon-viniferin, of their acetylated forms (resveratrol triacetate, epsilon-viniferin pentaacetate) and of vineatrol (a wine grape extract) were compared on human adenocarcinoma colon cells. Resveratrol and resveratrol triacetate inhibit cell proliferation and arrest cell cycle. epsilon-Viniferin and epsilon-viniferin pentaacetate slightly reduce cell proliferation. Vineatrol inhibits cell proliferation and favors an accumulation in the S phase of the ce…

Cell Membrane Permeabilityendocrine system diseasesvineatrolMESH: Cell CycleMESH: DNA ReplicationMESH: Flow CytometryresveratrolResveratrolMESH : Antineoplastic Agents PhytogenicWine grapechemistry.chemical_compoundMESH: Structure-Activity RelationshipMESH: StilbenesStilbenesMESH : Structure-Activity RelationshipMESH: Cell Membrane Permeabilityskin and connective tissue diseasesfood and beveragesDNA NeoplasmMESH : Cell DivisionCell cycleFlow CytometryMESH : Colonic Neoplasmscolon cancerBiochemistryColonic NeoplasmsMESH: Cell Divisioncell cycleMESH : DNA NeoplasmCell Divisionhormones hormone substitutes and hormone antagonistsMESH : DNA ReplicationBiotechnologyDNA ReplicationMESH: XenobioticsMESH: Cell Line TumorMESH : Flow CytometryMESH: Antineoplastic Agents PhytogenicMESH: DNA NeoplasmMESH : XenobioticsBiologyXenobioticsMESH : StilbenesStructure-Activity RelationshipCell Line TumorMESH : Cell Cycle[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyHumansStructure–activity relationship[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologypolyphenolsS phaseMESH: Colonic NeoplasmsMESH: HumansMESH : Cell Line TumorCell growthorganic chemicalsMESH : HumansAntineoplastic Agents PhytogenicchemistryMESH : Cell Membrane PermeabilityAcetylationCell cultureCancer researchFood ScienceMolecular Nutrition & Food Research
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