Search results for " Drug"

showing 10 items of 3138 documents

O6-methylguanine-DNA methyltransferase activity and sensitivity to cyclophosphamide and cisplatin in human lung tumor xenografts

1998

The DNA repair protein O6-methylguanine-DNA methyl-transferase (MGMT) is a main determinant of resistance of cells to the cytostatic effects of O6-alkylguanine-generating alkylating agents. The purpose of our study was to assay MGMT activity in cells of lung cancers and to correlate MGMT levels with chemotherapy response to cyclophosphamide (CTX) and cisplatin (DDP). MGMT levels were determined in 14 human lung tumor xenografts. There was a wide variation of MGMT expression in these tumors, ranging from 10 to 984 fmol/mg protein. There was also a wide range in the sensitivity of the xenografts to CTX and DDP, as measured by specific growth delay. When the MGMT levels of the different xenogr…

Cancer ResearchPathologymedicine.medical_specialtyLung NeoplasmsMethyltransferaseCyclophosphamidemedicine.medical_treatmentTransplantation HeterologousMice NudeAntineoplastic AgentsBiologyMiceO(6)-Methylguanine-DNA Methyltransferasechemistry.chemical_compoundIn vivoCarcinoma Non-Small-Cell LungCarcinomamedicineAnimalsHumansCyclophosphamideneoplasmsCisplatinChemotherapyDose-Response Relationship DrugO-6-methylguanine-DNA methyltransferasemedicine.diseasedigestive system diseasesNitrogen mustardOncologychemistryCancer researchFemaleCisplatinmedicine.drugInternational Journal of Cancer
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Phase I Assessment of New Mechanism-Based Pharmacodynamic Biomarkers for MLN8054, a Small-Molecule Inhibitor of Aurora A Kinase

2011

Abstract The mitotic kinase Aurora A is an important therapeutic target for cancer therapy. This study evaluated new mechanism-based pharmacodynamic biomarkers in cancer patients in two phase I studies of MLN8054, a small-molecule inhibitor of Aurora A kinase. Patients with advanced solid tumors received MLN8054 orally for 7 consecutive days in escalating dose cohorts, with skin and tumor biopsies obtained before and after dosing. Skin biopsies were evaluated for increased mitotic cells within the basal epithelium. Tumor biopsies were assessed for accumulation of mitotic cells within proliferative tumor regions. Several patients in the highest dose cohorts showed marked increases in the ski…

Cancer ResearchPathologymedicine.medical_specialtyMitotic indexBiopsyAurora A kinaseMitosisProtein Serine-Threonine KinasesBiologyBasal (phylogenetics)Aurora kinaseAurora KinasesNeoplasmsBiopsyBiomarkers TumormedicineHumansMitosisSkinDose-Response Relationship Drugmedicine.diagnostic_testCancerBenzazepinesmedicine.diseaseEpitheliummedicine.anatomical_structureOncologyCancer researchCancer Research
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Resveratrol-mediated apoptosis of hodgkin lymphoma cells involves SIRT1 inhibition and FOXO3a hyperacetylation

2012

Resveratrol (RSV), a plant-derived stilbene, induces cell death in Hodgkin lymphoma (HL)-derived L-428 cells in a dose-dependent manner (IC50 = 27 μM, trypan blue exclusion assay). At a lower range (25 μM), RSV treatment for 48 hr causes arrest in the S-phase of the cell cycle, while at a higher concentration range (50 μM), apoptosis can be detected, with activation of caspase-3. The histone/protein deacetylase SIRT1 has been described as a putative target of RSV action in other model systems, even though its role in cancer cells is still controversial. Here we show that RSV, at both concentration ranges, leads to a marked increase in p53, while a decrease of SIRT1 expression level, as well…

Cancer ResearchPathologymedicine.medical_specialtyProgrammed cell deathApoptosisCell Growth ProcessesBiologyS PhaseSirtuin 1Cell Line TumorStilbenesmedicineHumansbcl-2-Associated X ProteinB-LymphocytesDose-Response Relationship DrugCaspase 3Mantle zoneForkhead Box Protein O3Germinal centerAcetylationForkhead Transcription FactorsCell cycleGerminal CenterHodgkin DiseaseMolecular biologyOncologyResveratrolCell cultureApoptosisCancer cellLymph NodesLymphTumor Suppressor Protein p53International Journal of Cancer
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Development of resistance towards artesunate in MDA-MB-231 human breast cancer cells.

2011

Breast cancer is the most common cancer and the second leading cause of cancer death in industrialized countries. Systemic treatment of breast cancer is effective at the beginning of therapy. However, after a variable period of time, progression occurs due to therapy resistance. Artesunate, clinically used as anti-malarial agent, has recently revealed remarkable anti-tumor activity offering a role as novel candidate for cancer chemotherapy. We analyzed the anti-tumor effects of artesunate in metastasizing breast carcinoma in vitro and in vivo. Unlike as expected, artesunate induced resistance in highly metastatic human breast cancer cells MDA-MB-231. Likewise acquired resistance led to abol…

Cancer ResearchPhytochemistryPhytopharmacologyCancer TreatmentArtesunateApoptosisElectrophoretic Mobility Shift AssayDrug resistanceNude MiceMetastasischemistry.chemical_compoundMiceMolecular Cell BiologyDrug DiscoveryBreast TumorsBasic Cancer ResearchMedicinebcl-2-Associated X ProteinMultidisciplinaryQRNF-kappa BArtemisininsChemistryOncologyMedicineFemaleMatrix Metalloproteinase 1Breast carcinomamedicine.drugResearch Article570Drugs and DevicesDrug Research and DevelopmentCell SurvivalScienceMice Nude570 Life SciencesBreast NeoplasmsTumor Cell Line610 Medical Sciences MedicineBreast cancerComplementary and Alternative MedicineCell Line TumorAnimalsHumansDoxorubicinBiologyNeoplasm Drug Resistancebusiness.industryCancers and NeoplasmsChemotherapy and Drug Treatmentmedicine.diseaseXenograft Model Antitumor AssaysTranscription Factor AP-1chemistryTumor progressionArtesunateDrug Resistance NeoplasmCancer cellImmunologyEthnopharmacologyCancer researchbusinessPloS one
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Downregulation of RhoB GTPase confers resistance to cisplatin in human larygneal carcinoma cells

2009

Acquired resistance to cisplatin represents a major obstacle to an efficient chemotherapy. We found downregulation of RhoB expression in cisplatin-resistant tumor cell lines from different origin. In cisplatin-resistant laryngeal carcinoma subline overexpression of farnesylated or geranylgeranylated RhoB increased cisplatin-induced cell death, while silencing of RhoB expression diminished sensitivity of parental HEp-2 cells via decreased cellular accumulation of cisplatin. However, since RhoB silencing in additional tumor cell lines did not alter their sensitivity to cisplatin, we can assume that RhoB downregulation does not provide general protective role in cell response to cisplatin. Nev…

Cancer ResearchProgrammed cell deathGenetic enhancementRHOBmedicine.medical_treatmentDown-RegulationAntineoplastic AgentsBiologyDownregulation and upregulationCell Line TumormedicineCarcinomaHumansGene silencingrhoB GTP-Binding ProteinLaryngeal NeoplasmsCisplatinChemotherapymedicine.diseaseCell biologyOncologyDrug Resistance NeoplasmCancer researchcisplatin ; drug resistance ; Rho GTPases ; RhoBCisplatinmedicine.drug
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In vivo effects of tumor necrosis factor-α or flavone acetic acid in combination with doxorubicin on multidrug-resistant B16 melanoma

1996

Having observed that tumor necrosis factor (TNF)-alpha and doxorubicin (DXR) produce a synergistic inhibition of melanoma B16 and also of its multidrug resistant (MDR) variant in vitro, we tested whether this interaction would occur in vivo as well. C57BL/6 mice with s.c. tumors were treated with TNF or flavone acetic acid (FAA), a biological response modifier, in simultaneous or sequential combination with DXR. The agents were administered systemically. Overall, the results were negative, apart from a trend towards slight synergy, found in the chemosensitive melanoma, when TNF was given 1 or 2 days before DXR. The effects of FAA and DXR were found to be subadditive or antagonistic. However…

Cancer ResearchSkin NeoplasmsMelanoma ExperimentalMiceIn vivoAntineoplastic Combined Chemotherapy ProtocolsmedicineAnimalsPharmacology (medical)DoxorubicinFlavonoidsPharmacologyAntibiotics AntineoplasticFlavone acetic acidDose-Response Relationship DrugTumor Necrosis Factor-alphaChemistryMelanomamedicine.diseaseDrug Resistance MultipleIn vitroMultiple drug resistanceOncologyBiochemistryDoxorubicinDrug Resistance NeoplasmCancer researchFemaleTumor necrosis factor alphaB16 melanomamedicine.drugAnti-Cancer Drugs
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Tumor-initiating activity of the (+)-(S,S)- and (−)-(R,R)-enantiomers of trans-11,12-dihydroxy-11,12-dihydrodibenzo[a,l]pyrene in mouse skin

1999

Abstract A single administration of enantiomerically pure 11,12-dihydrodiols of dibenzo[ a,l ]pyrene (DB[ a,l ]P) on the back of NMRI mice and subsequent chronic treatment with 12- O -tetradecanoylphorbol 13-acetate (TPA) (initiation/promotion assay) revealed strikingly different carcinogenic activities of both enantiomers. Tumor-initiating activity of (−)-(11 R ,12 R )-DB[ a,l ]P-dihydrodiol, which is the metabolic precursor of the (−)- anti -(11 R ,12 S )-dihydrodiol (13 S ,14 R )-epoxide, was exceptionally higher than the corresponding effect of (+)-(11 S ,12 S )-DB[ a,l ]P-dihydrodiol, the metabolic precursor of (+)- syn -(11 S ,12 R )-dihydrodiol (13 S ,14 R )-epoxide. After topical ap…

Cancer ResearchSkin NeoplasmsTime FactorsCarcinogenicity TestsStereochemistryEpoxideTumor initiationmedicine.disease_causeMicechemistry.chemical_compoundpolycyclic compoundsmedicineAnimalsBenzopyransCarcinogenCarcinogenic Polycyclic Aromatic HydrocarbonDose-Response Relationship DrugChemistryStereoisomerismSurvival RateOncologyBiochemistryCarcinogensPyreneFemaleStereoselectivityEnantiomerGenotoxicityCancer Letters
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LS104, a non-ATP-competitive small-molecule inhibitor of JAK2, is potently inducing apoptosis in JAK2V617F-positive cells

2008

Abstract The activating JAK2V617F mutation has been described in the majority of patients with BCR-ABL-negative myeloproliferative disorders (MPD). In this report, we characterize the small-molecule LS104 as a novel non-ATP-competitive JAK2 inhibitor: Treatment of JAK2V617F-positive cells with LS104 resulted in dose-dependent induction of apoptosis and inhibition of JAK2 autophosphorylation and of downstream targets. Activation of these targets by JAK2 was confirmed in experiments using small interfering RNA. LS104 inhibited JAK2 kinase activity in vitro. This effect was not reversible using elevated ATP concentrations, whereas variation of the kinase substrate peptide led to modulation of …

Cancer ResearchSmall interfering RNAApoptosisStyrenesMiceAdenosine TriphosphateCell Line Tumorhemic and lymphatic diseasesAnimalsHumansPhosphorylationKinase activityProtein Kinase InhibitorsMyeloproliferative DisordersJanus kinase 2AcrylonitrileDose-Response Relationship DrugbiologyKinaseAutophosphorylationJanus Kinase 2Molecular biologyIn vitroOncologyApoptosisbiology.proteinSignal transductionK562 CellsSignal TransductionMolecular Cancer Therapeutics
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Gonadotropin-releasing hormone agonist for the prevention of chemotherapy-induced ovarian failure in patients with lymphoma: 1-year follow-up of a pr…

2013

PURPOSE To assess the efficacy of gonadotropin-releasing hormone agonist (GnRHa) in preventing chemotherapy-induced ovarian failure in patients treated for Hodgkin or non-Hodgkin lymphoma within the setting of a multicenter, randomized, prospective trial. PATIENTS AND METHODS Patients age 18 to 45 years were randomly assigned to receive either the GnRHa triptorelin plus norethisterone (GnRHa group) or norethisterone alone (control group) concomitantly with alkylating agents containing chemotherapy. The primary end point was the premature ovarian failure (POF) rate (follicle-stimulating hormone [FSH] ≥ 40 IU/L) after 1 year of follow-up. Results Eighty-four of 129 randomly assigned patients …

Cancer ResearchTime FactorsLymphomamedicine.medical_treatmentGonadotropin-Releasing Hormone -- agonistsPrimary Ovarian InsufficiencyTriptorelin Pamoate -- therapeutic uselaw.inventionGonadotropin-Releasing HormoneGynécologieRandomized controlled triallawAntineoplastic Combined Chemotherapy ProtocolsClinical endpointBiological Markers -- bloodNorethindrone -- therapeutic useProspective StudiesTreatment FailureProspective cohort studyTriptorelin PamoateEstradiolLymphoma Non-HodgkinLymphoma -- drug therapyMiddle AgedTriptorelinHodgkin DiseasePremature ovarian failureLuteolytic AgentsOncologyHodgkin Disease -- drug therapyDrug Therapy CombinationFemaleEstradiol -- bloodmedicine.drugAdultAntineoplastic Combined Chemotherapy Protocols -- administration & dosage -- adverse effectsmedicine.medical_specialtyNorethisteronemedicine.drug_classUrologyFollicle Stimulating Hormone -- bloodGonadotropin-releasing hormone agonistmedicineHumansGynecologyChemotherapybusiness.industrymedicine.diseaseLuteolytic Agents -- therapeutic useCancérologieLymphoma Non-Hodgkin -- drug therapyPremenopausePrimary Ovarian Insufficiency -- blood -- chemically induced -- prevention & controlFollicle Stimulating HormoneNorethindronebusinessBiomarkersFollow-Up Studies
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MUC1 oncoprotein promotes refractoriness to chemotherapy in thyroid cancer cells.

2007

Abstract Overexpression of MUC1 oncoprotein is frequently observed in cancer and contributes to confer resistance to genotoxic agents. Papillary, follicular, and anaplastic thyroid carcinomas are the three forms of thyroid epithelial cancer. Anaplastic tumors are less differentiated and extremely aggressive, characterized by a poor prognosis. Little is known about the role of MUC1 in thyroid cancer. We recently showed that autocrine production of interleukin (IL)-4 and IL-10 controls thyroid cancer cell survival, growth, and resistance to chemotherapy through activation of Janus-activated kinase/signal transducers and activators of transcription (JAK/STAT) and phosphatidylinositide 3′-OH ki…

Cancer ResearchTranscription GeneticDrug ResistanceApoptosisSuppressor of Cytokine Signaling ProteinsnPhosphatidylinositol 3-KinasesAntibioticsMedicineRNA Small InterferingThyroid cancerTumorAntibiotics AntineoplasticThyroidAntineoplasticInterleukin-10Mitochondriamedicine.anatomical_structureOncologyTranscriptionSignal TransductionDown-RegulationSmall InterferingTransfectionCell LineThyroid carcinomaSuppressor of Cytokine Signaling 1 ProteinGeneticSettore MED/04 - PATOLOGIA GENERALEAntigens NeoplasmCell Line TumorHumansThyroid NeoplasmsAnaplastic thyroid cancerAntigensProtein kinase BPI3K/AKT/mTOR pathwayAntibiotics Antineoplastic; Antigens Neoplasm; Apoptosis; Cell Line Tumor; Down-Regulation; Doxorubicin; Drug Resistance Neoplasm; Humans; Interleukin-10; Interleukin-4; Mitochondria; Mucin-1; Mucins; Phosphatidylinositol 3-Kinases; Proto-Oncogene Proteins c-akt; RNA Small Interfering; Signal Transduction; Suppressor of Cytokine Signaling 1 Protein; Suppressor of Cytokine Signaling Proteins; Thyroid Neoplasms; Transcription Genetic; Transfection; Cancer Research; Oncologybusiness.industryMucin-1MucinsCancermedicine.diseaseDoxorubicinDrug Resistance NeoplasmCancer cellCancer researchNeoplasmRNAInterleukin-4businessProto-Oncogene Proteins c-aktCancer research
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