Search results for "Azine"

showing 10 items of 1589 documents

Prospective Study of the Evolution of Blood Lymphoid Immune Parameters during Dacarbazine Chemotherapy in Metastatic and Locally Advanced Melanoma Pa…

2014

BackgroundThe importance of immune responses in the control of melanoma growth is well known. However, the implication of these antitumor immune responses in the efficacy of dacarbazine, a cytotoxic drug classically used in the treatment of melanoma, remains poorly understood in humans.MethodsIn this prospective observational study, we performed an immunomonitoring of eleven metastatic or locally advanced patients treated with dacarbazine as a first line of treatment. We assessed by flow cytometry lymphoid populations and their activation state; we also isolated NK cells to perform in vitro cytotoxicity tests.ResultsWe found that chemotherapy induces lymphopenia and that a significantly hig…

CD4-Positive T-LymphocytesMaleSkin Neoplasmsmedicine.medical_treatmentCancer TreatmentGene ExpressionNK cellsLymphocyte ActivationT-Lymphocytes RegulatoryLeukocyte CountCellular typesMedicine and Health SciencesCytotoxic T cellProspective StudiesNeoplasm MetastasisProspective cohort studyImmune ResponseMelanomaAged 80 and overMultidisciplinarymedicine.diagnostic_testReverse Transcriptase Polymerase Chain ReactionMelanomaQRMiddle AgedFlow CytometryPrognosis3. Good healthDacarbazineKiller Cells NaturalTreatment OutcomeOncologyCutaneous MelanomaMedicineWhite blood cellsFemaleImmunotherapymedicine.drugResearch ArticleTumor ImmunologyAdultCell biologyBlood cellsCell SurvivalDacarbazineScienceImmune CellsImmunologyLocally advancedT cellsMalignant Skin NeoplasmsDermatologyCancer ImmunotherapyFlow cytometryImmune systemCell Line TumormedicineHumansAntineoplastic Agents AlkylatingAgedChemotherapyBiology and life sciencesbusiness.industrymedicine.diseaseAnimal cellsImmunologyCancer researchClinical ImmunologybusinessTranscription FactorsPLoS ONE
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Novel pathway in Bcr-Abl signal transduction involves Akt-independent, PLC-γ1-driven activation of mTOR/p70S6-kinase pathway

2009

In chronic myeloid leukemia, activation of the phosphoinositide 3-kinase (PI3K)/Akt pathway is crucial for survival and proliferation of leukemic cells. Essential downstream molecules involve mammalian target of rapamycin (mTOR) and S6-kinase. Here, we present a comprehensive analysis of the molecular events involved in activation of these key signaling pathways. We provide evidence for a previously unrecognized phospholipase C-gamma1 (PLC-gamma1)-controlled mechanism of mTOR/p70S6-kinase activation, which operates in parallel to the classical Akt-dependent machinery. Short-term imatinib treatment of Bcr-Abl-positive cells caused dephosphorylation of p70S6-K and S6-protein without inactivat…

Cancer ResearchBlotting WesternMedizinFusion Proteins bcr-ablApoptosisProtein Serine-Threonine KinasesBiologyPiperazinesMiceLeukemia Myelogenous Chronic BCR-ABL Positivehemic and lymphatic diseasesGeneticsAnimalsHumansRNA Small InterferingProtein Kinase InhibitorsMolecular BiologyProtein kinase BCAMKPI3K/AKT/mTOR pathwayPhospholipase C gammaCell growthKinaseTOR Serine-Threonine KinasesRPTORIntracellular Signaling Peptides and ProteinsRibosomal Protein S6 Kinases 70-kDaCell biologyEnzyme ActivationPyrimidinesBenzamidesembryonic structuresImatinib MesylateCancer researchPhosphorylationSignal transductionProto-Oncogene Proteins c-aktSignal TransductionOncogene
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SAHA induces apoptosis in hepatoma cells and synergistically interacts with the proteasome inhibitor Bortezomib.

2007

Histone deacetylase (HDAC) inhibitors represent a promising group of anticancer agents. This paper shows that the HDAC inhibitor suberoylanilide hydroxamic acid (SAHA) stimulated at 5-10 microM apoptosis in human hepatoma HepG2 and Huh6 cells, but was ineffective in primary human hepatocytes (PHH). In HepG2 cells SAHA induced the extrinsic apoptotic pathway, increasing the expression of both FasL and FasL receptor and causing the activation of caspase-8. Moreover, SAHA enhanced the level of Bim proteins, stimulated alternative splicing of the Bcl-X transcript with the expression of the proapoptotic Bcl-Xs isoform, induced degradation of Bid into the apoptotic factor t-Bid and dephosphorylat…

Cancer ResearchCarcinoma HepatocellularFas Ligand ProteinClinical BiochemistryPharmaceutical ScienceApoptosisHydroxamic AcidsFas ligandHistone DeacetylasesBortezomibCell Line TumormedicineHumansProtease InhibitorsProtein kinase BVorinostatHDAC inhibitors . HepG2 cells . PHH . Extrinsic and intrinsic apoptotic pathwaysbcl-2-Associated X ProteinPharmacologyMembrane Potential MitochondrialCaspase 8VorinostatbiologyChemistryBortezomibCytochrome cBiochemistry (medical)Cell BiologyBoronic AcidsHistone Deacetylase InhibitorsProteasomeApoptosisPyrazinesProteasome inhibitorbiology.proteinCancer researchApoptosis Regulatory ProteinsProteasome Inhibitorsmedicine.drug
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Bortezomib: a new pro-apoptotic agent in cancer treatment.

2010

Bortezomib is a proteasome inhibitor. It targets the ubiquitin-proteasome pathway with subsequent inhibition of the degradation of proteins involved in cell cycle regulation and cancer cell survival. The best known molecular mechanism concerns the inhibition of IkappaB breakdown and the related stabilization of NFkappaB, thus preventing its translocation to the nucleus for the activation of downstream pathways. Bortezomib is the only drug in this class which has been approved for clinical use. It has shown an efficient antitumor effect in a phase III clinical trial (APEX) involving relapsed multiple myeloma patients. Response rate, time to progression and overall survival have been improved…

Cancer ResearchCell cycle checkpointSettore MED/06 - Oncologia MedicaAntineoplastic AgentsApoptosisPharmacologyDexamethasoneBortezomibMiceNeoplasmshemic and lymphatic diseasesAntineoplastic Combined Chemotherapy ProtocolsDrug DiscoverymedicineAnimalsHumansDexamethasoneMultiple myelomaPharmacologyproteasome inhibitionClinical Trials as TopicNeovascularization Pathologicbusiness.industryBortezomibCell CycleNF-kappa Bsolid tumorsmedicine.diseaseBoronic AcidsClinical trialBortezomib; solid tumors; proteasome inhibition.OncologyApoptosisPyrazinesCancer cellProteasome inhibitorCancer researchMultiple MyelomabusinessProteasome InhibitorsBortezomib solid tumors proteasome inhibitionmedicine.drug
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A sphingosine kinase inhibitor combined with temozolomide induces glioblastoma cell death through accumulation of dihydrosphingosine and dihydroceram…

2014

AbstractGlioblastomas (GBMs) are very aggressive tumors with low chemosensitivity. The DNA-alkylating agent temozolomide (TMZ) is currently the most efficient chemotoxic drug for GBM therapy; however, many patients develop resistance to TMZ. Combining TMZ with another agent could present an improved treatment option if it could overcome TMZ resistance and avoid side effects. Sphingosine kinase inhibitors (SKIs) have emerged as anticancer agents. Sphingosine kinases are often overexpressed in tumors where their activity of phosphorylating sphingosine (Sph) contributes to tumor growth and migration. They control the levels of the pro-apoptotic ceramide (Cer) and Sph and of the pro-survival sp…

Cancer ResearchCeramideProgrammed cell deathImmunologySphingosine kinaseAntineoplastic AgentsApoptosisBiologyCeramidesCellular and Molecular Neurosciencechemistry.chemical_compoundSphingosineCell Line TumorAutophagyTemozolomideHumansEnzyme InhibitorsCytotoxicitySphingosineCell DeathKinaseBrain NeoplasmsAutophagyCell BiologyEndoplasmic Reticulum StressCell biologyDacarbazinePhosphotransferases (Alcohol Group Acceptor)chemistryApoptosisDrug Resistance NeoplasmCancer researchDrug Therapy CombinationOriginal ArticleGlioblastomaCell deathdisease
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The new iodoacetamidobenzofuran derivative TR120 decreases STAT5 expression and induces antitumor effects in imatinib-sensitive and imatinib-resistan…

2013

The identification of novel compounds modulating the expression/activity of molecular targets downstream to BCR-ABL could be a new approach in the treatment of chronic myeloid leukemias (CMLs) resistant to imatinib or other BCR-ABL-targeted molecules. Recently, we synthesized a new class of substituted 2-(3,4,5-trimethoxybenzoyl)-2-N,N-dimethylamino-benzo[b]furans, and among these 3-iodoacetylamino-6-methoxybenzofuran-2-yl(3,5-trimethoxyphenyl)methanone (TR120) showed marked cytotoxic activity in BCR-ABL-expressing cells. Interestingly, TR120 was more potent than imatinib in cell growth inhibition and apoptosis induction in both BCR-ABL-expressing K562 and KCL22 cells. Moreover, it showed a…

Cancer ResearchFusion Proteins bcr-ablApoptosisPiperazinesSettore MED/15 - Malattie Del Sanguechemistry.chemical_compoundhemic and lymphatic diseasesSTAT5 Transcription FactorCytotoxic T cellPharmacology (medical)Cyclin D1STAT5biologyDrug SynergismCell cycleNeoplasm ProteinsGene Expression Regulation NeoplasticLeukemiaOncologyProto-Oncogene Proteins c-bcl-2BenzamidesImatinib MesylateGrowth inhibitionmedicine.drugbcl-X ProteinDown-RegulationAntineoplastic AgentsBone Marrow CellsResting Phase Cell CycleColony-Forming Units AssayBenzophenonesNecrosisCell Line TumorLeukemia Myelogenous Chronic BCR-ABL PositivemedicineHumansneoplasmsBenzofuransPharmacologyG1 PhaseImatinibBCR-ABL chronic myeloid leukemia imatinib resistance STAT5 tyrosine kinase inhibitorsmedicine.diseaseSettore CHIM/08 - Chimica FarmaceuticaGenes bcl-1Genes bcl-2PyrimidineschemistryApoptosisDrug Resistance NeoplasmSettore BIO/14 - FarmacologiaCancer researchbiology.proteinK562 CellsK562 cells
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Pimasertib Versus Dacarbazine in Patients With Unresectable NRAS-Mutated Cutaneous Melanoma: Phase II, Randomized, Controlled Trial with Crossover

2020

This study investigated the efficacy and safety of pimasertib (MEK1/MEK2 inhibitor) versus dacarbazine (DTIC) in patients with untreated NRAS-mutated melanoma. Phase II, multicenter, open-label trial. Patients with unresectable, stage IIIc/IVM1 NRAS-mutated cutaneous melanoma were randomized 2:1 to pimasertib (60 mg

Cancer ResearchGastroenterologypimasertiblaw.invention0302 clinical medicineRandomized controlled triallawClinical endpoint030212 general & internal medicineMalignant melanomaHazard ratioProgression-free survivalSciences bio-médicales et agricoleslcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens3. Good healthDacarbazineOncology[SDV.SP.PHARMA] Life Sciences [q-bio]/Pharmaceutical sciences/Pharmacology030220 oncology & carcinogenesismedicine.symptomPimasertibmedicine.drugQuality of lifemedicine.medical_specialtyNauseaDacarbazinemalignant melanomadacarbazine[SDV.CAN]Life Sciences [q-bio]/CancerN-(2 3-dihydroxypropyl)-1-((2-fluoro-4-iodophenyl)amino)isonicotinamideNeutropeniaN-(23-dihydroxypropyl)-1-((2-fluoro-4-iodophenyl)amino)isonicotinamidelcsh:RC254-282Article03 medical and health sciences[SDV.CAN] Life Sciences [q-bio]/CancerInternal medicinemedicineProgression-free survivalAdverse effectbusiness.industry[SDV.MHEP.DERM] Life Sciences [q-bio]/Human health and pathology/Dermatologymedicine.diseaseadverse eventsCancérologiequality of lifeAdverse events[SDV.SP.PHARMA]Life Sciences [q-bio]/Pharmaceutical sciences/Pharmacologybusinessprogression-free survival[SDV.MHEP.DERM]Life Sciences [q-bio]/Human health and pathology/Dermatology
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Selectivity analysis of protein kinase CK2 inhibitors DMAT, TBB and resorufin in cisplatin-induced stress responses.

2009

Udgivelsesdato: 2009-Nov Targeting protein kinases as a therapeutic approach to treat various diseases, especially cancer is currently a fast growing business. Although many inhibitors are available, exhibiting remarkable potency, the major challenge is their selectivity. Here we show that the protein kinase CK2 inhibitors DMAT, TBB and resorufin differ in their selectivity against PI3K family members, since PI3K and DNA-PK are subject to inhibition by DMAT and TBB, however, not by resorufin. TBB and DMAT treatment together with cisplatin lead to an inhibition of cisplatin-induced stress signaling (as detected by phosphorylation of JNK and H2AX). In the case of resorufin no interference wit…

Cancer ResearchKinaseCell SurvivalBlotting WesternAntineoplastic AgentsCell cycleBiologyTriazolesCell killingOncologyBiochemistryApoptosisStress PhysiologicalCell Line TumorOxazinesPhosphorylationHumansBenzimidazolesViability assayCasein kinase 2Signal transductionCisplatinEnzyme InhibitorsCasein Kinase IISignal TransductionInternational journal of oncology
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WIN induces apoptotic cell death in human colon cancer cells through a block of autophagic flux dependent on PPARγ down-regulation.

2014

Cannabinoids have been reported to possess anti-tumorigenic activity in cancer models although their mechanism of action is not well understood. Here, we show that the synthetic cannabinoid WIN55,212-2 (WIN)-induced apoptosis in colon cancer cell lines is accompanied by endoplasmic reticulum stress induction. The formation of acidic vacuoles and the increase in LC3-II protein indicated the involvement of autophagic process which seemed to play a pro-survival role against the cytotoxic effects of the drug. However, the enhanced lysosomal membrane permeabilization (LMP) blocked the autophagic flux after the formation of autophagosomes as demonstrated by the accumulation of p62 and LC3, two ma…

Cancer ResearchMorpholinesClinical BiochemistryPharmaceutical ScienceDown-RegulationAntineoplastic AgentsApoptosisBiologyNaphthalenesDownregulation and upregulationSettore BIO/10 - BiochimicaCell Line TumormedicineAutophagyGene silencingHumansViability assayPharmacologyEndoplasmic reticulumBiochemistry (medical)AutophagyCannabinoids PPARγ ER stress autophagy/apoptosis interplay colon carcinoma cellsCell BiologyEndoplasmic Reticulum StressCell biologyBenzoxazinesMitochondriaPPAR gammaMechanism of actionApoptosisColonic NeoplasmsUnfolded protein responsemedicine.symptomSignal TransductionApoptosis : an international journal on programmed cell death
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The dual PI3K/mTOR inhibitor PKI-587 enhances sensitivity to cetuximab in EGFR-resistant human head and neck cancer models

2014

Background:Cetuximab is the only targeted agent approved for the treatment of head and neck squamous cell carcinomas (HNSCC), but low response rates and disease progression are frequently reported. As the phosphoinositide 3-kinase (PI3K) and the mammalian target of rapamycin (mTOR) pathways have an important role in the pathogenesis of HNSCC, we investigated their involvement in cetuximab resistance.Methods:Different human squamous cancer cell lines sensitive or resistant to cetuximab were tested for the dual PI3K/mTOR inhibitor PF-05212384 (PKI-587), alone and in combination, both in vitro and in vivo.Results:Treatment with PKI-587 enhances sensitivity to cetuximab in vitro, even in the co…

Cancer ResearchPathologyCetuximabApoptosisHNSCCHNSCCMiceAntineoplastic Combined Chemotherapy ProtocolsNeoplasmPhosphoinositide-3 Kinase InhibitorsMice Inbred BALB CCetuximabCaspase 3TriazinesTOR Serine-Threonine KinasesCetuximab resistanceErbB ReceptorsOncologyHead and Neck NeoplasmsMonoclonalCarcinoma Squamous Cellmedicine.drugmedicine.medical_specialtyMorpholinesPI3K-mTOR inhibitorsMice NudeAntineoplastic AgentsBiologyAntibodies Monoclonal HumanizedCell Line TumorAutophagymedicineCarcinomaAnimalsHumansneoplasmsPI3K/AKT/mTOR pathwayCell Proliferationcetuximab resistanceSquamous Cell Carcinoma of Head and Necktarget therapyCell growthAutophagyCancermedicine.diseaseXenograft Model Antitumor Assaysdigestive system diseasesDrug Resistance NeoplasmPI3K7mTOR inhibitorsCancer researchTranslational TherapeuticsBritish Journal of Cancer
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