Search results for "relation"

showing 10 items of 10542 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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Lovastatin protects human endothelial cells from killing by ionizing radiation without impairing induction and repair of DNA double-strand breaks.

2006

Abstract Purpose: 3-hydroxy-3-methylglutaryl CoA reductase inhibitors (statins) are frequently used lipid-lowering drugs. Moreover, they are reported to exert pleiotropic effects on cellular stress responses, proliferation, and apoptosis. Whether statins affect the sensitivity of primary human cells to ionizing radiation (IR) is still unknown. The present study aims at answering this question. Experimental Design: The effect of lovastatin on IR-provoked cytotoxicity was analyzed in primary human umbilical vein endothelial cells (HUVEC). To this end, cell viability, proliferation, and apoptosis as well as DNA damage–related stress responses were investigated. Results: The data show that lova…

Cancer ResearchProgrammed cell deathDNA RepairDNA repairDNA damageCell SurvivalApoptosisRadioresistanceRadiation Ionizingpolycyclic compoundsmedicineHumansLovastatinCells CulturedCell Proliferationbiologynutritional and metabolic diseasesEndothelial CellsDose-Response Relationship RadiationDNAMolecular biologyEndothelial stem cellOncologyApoptosisCytoprotectionHMG-CoA reductasebiology.proteinCancer researchlipids (amino acids peptides and proteins)Lovastatinmedicine.drugDNA DamageClinical cancer research : an official journal of the American Association for Cancer Research
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Wavelength dependence of oxidative DNA damage induced by UV and visible light.

1997

DNA damage induced by UV radiation and visible light (290-500 nm) in AS52 Chinese hamster cells was analysed by an alkaline elution assay with specific repair endonucleases. Cells were exposed to extensively filtered monochrome or broad-band radiation. Between 290 and 315 nm, the ratio of base modifications sensitive to Fpg protein (i.e. 8-hydroxyguanine and formamidopyrimidines) and T4 endonuclease V (i.e. cyclobutane pyrimidine dimers) was constant (approximately 1:200), indicating that the direct excitation of DNA is responsible for both types of damage in this range of the spectrum. While the yield of pyrimidine dimers per unit dose continued to decrease exponentially beyond 315 nm, the…

Cancer ResearchPyrimidinebiologyLightSinglet oxygenDNA damageUltraviolet RaysPyrimidine dimerDose-Response Relationship RadiationGeneral MedicineCHO CellsPhotochemistrymedicine.disease_causechemistry.chemical_compoundEndonucleaseOxidative StresschemistryCricetinaebiology.proteinmedicineAnimalsDNAOxidative stressVisible spectrumDNA DamageCarcinogenesis
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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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Foreword: Implementing cancer prevention in Europe

2010

The understanding of risk factors underpinning the aetiology of many common cancers is well established, yet the conversion of this knowledge into prevention lags considerably behind. The title of this Special Issue - Implementing cancer prevention in Europe - captures the central theme within; namely, the translation of cancer epidemiology into public health policy. The Special Issue is supported by focused evidence-based case studies of how these processes might be best taken forward. (C) 2010 Published by Elsevier Ltd.

Cancer ResearchUnderpinningCancer preventionOncologySDG 3 - Good Health and Well-beingbusiness.industryEpidemiology of cancerMedicinePublic relationsbusinessPublic health policyTheme (narrative)European Journal of Cancer
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Differential inhibition of renal cancer cell invasion mediated by fibronectin, collagen IV and laminin.

2000

Invasion of tumor cells into the extracellular matrix is an essential step in the formation of metastases in renal cancer. Cell adhesion molecules such as beta(1)-integrins, which bind to the RGD sequence (arginine-glycine-asparagine) and CD44 are involved in this process. We examined the invasion of a renal carcinoma cell line (CCF-RC1) into the extracellular matrix compounds fibronectin, collagen IV and laminin and the effect of TGFbeta and IFNgamma on this process. The inhibitory effect of an antibody against the beta(1)-subunit of integrins (CD29), as well as a pentapeptide including the RGD sequence, was also evaluated. A micro-chemotaxis chamber, including a polycarbonate membrane wit…

Cancer Researchmedicine.medical_specialtyIntegrinExtracellular matrixInterferon-gammaLamininCell MovementTransforming Growth Factor betaInternal medicinemedicineTumor Cells CulturedHumansNeoplasm InvasivenessCarcinoma Renal CellbiologyDose-Response Relationship DrugCell adhesion moleculeChemotaxisIntegrin beta1CD44Cell migrationCD29Kidney NeoplasmsCell biologyExtracellular MatrixFibronectinsFibronectinEndocrinologyHyaluronan ReceptorsOncologybiology.proteinCollagenLamininOligopeptidesCancer letters
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