Search results for "growth"

showing 10 items of 5134 documents

The synergistic apoptotic effects of thiophenfurin, an inosine monophosphate dehydrogenase inhibitor, in combination with retinoids in HL60 cells

2006

New effective cytotoxic agents and combinations are urgently needed in cancer treatment. The enzyme inosine monophosphate dehydrogenase is a potentially useful target for drug development, since its activity has been shown to be amplified in malignant cells. Thiophenfurin, an inhibitor of the enzyme synthesized by us, is endowed with a significant apoptotic activity in promyelocytic leukaemia HL60 cells. Since retinoids were successfully employed in the treatment of patients with leukaemia, demonstrating significant differentiation-inducing and apoptotic effects, we carried out this study to evaluate the effects of the combination of thiophenfurin and several retinoid molecules, acting in d…

Cancer Researchmedicine.drug_classCellApoptosisHL-60 CellsTretinoinCell Growth ProcessesBiologyInosine Monophosphate Dehydrogenase InhibitorIMP DehydrogenaseIMP dehydrogenaseTretinoinAntineoplastic Combined Chemotherapy ProtocolsmedicineHumansRetinoidEnzyme InhibitorsCytotoxicityMembrane Potential MitochondrialCell growthCell CycleDrug SynergismGeneral MedicineCell cycleMitochondriaenzymemedicine.anatomical_structureOncologyBiochemistryRibonucleosidesmedicine.drugOncology Reports
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Shikonin and its derivatives inhibit the epidermal growth factor receptor signaling and synergistically kill glioblastoma cells in combination with e…

2015

Overexpression and mutation of the epidermal growth factor receptor (EGFR) gene play a causal role in tumorigenesis and resistance to treatment of glioblastoma (GBM). EGFR inhibitors such as erlotinib are currently used for the treatment of GBM; however, their efficacy has been limited due to drug resistance. New treatment strategies are therefore urgently needed. Shikonin, a natural naphthoquinone, induces both apoptosis and necroptosis in human glioma cells, but the effectiveness of erlotinib-shikonin combination treatment as well as the underlying molecular mechanisms is unknown yet. In this study, we investigated erlotinib in combination with shikonin and 14 shikonin derivatives in pare…

Cancer Researchmedicine.drug_classNecroptosisBiologyPharmacologyTyrosine-kinase inhibitorrespiratory tract diseasesOncologyCell culturemedicineCancer researchbiology.proteinErlotinibEpidermal growth factor receptorCytotoxicityneoplasmsProtein kinase Bmedicine.drugEGFR inhibitorsInternational Journal of Cancer
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A first-in-human trial of RG7116, a glycoengineered monoclonal antibody targeting HER3, in patients with advanced/metastatic tumors of epithelial cel…

2013

2522 Background: The Human Epidermal Growth Factor Receptor 3 (HER3) is a key heterodimerization partner for other HER family members thereby acting as a downstream signal amplifier. This is a first in human study evaluating the safety of RG7116, a humanized anti-HER3 monoclonal antibody with potent HER3 signal inhibition. Due to a glycoengineered Fc-part this antibody displays enhanced antibody-dependent cellular cytotoxicity as compared to conventional antibodies. Methods: Patients (pts) with advanced or metastatic carcinomas with centrally confirmed HER3 protein expression were included. A “3+3” dose escalation design was performed starting at 100 mg flat dosing in a q2w regimen. In add…

Cancer Researchmedicine.drug_classbusiness.industryFirst in humanMonoclonal antibodyEpitheliumSignal amplifiermedicine.anatomical_structureOncologyDownstream (manufacturing)Cancer researchmedicineHuman epidermal growth factor receptorIn patientbusinessJournal of Clinical Oncology
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Abstract 1855: Role of mTOR inhibition in triple-negative breast cancer

2016

Abstract BACKGROUND: Triple-negative breast cancers (TNBC) represent the 10-17% of all diagnosed breast cancers (BC) and are characterized by the absence of ER/PgR expression, HER2 amplification and often show a basal-like phenotype. TNBC are often diagnosed in patients with BRCA1 germline mutation and unfortunately treatment options are still limited. The mTOR (Mammalian Target Of Rapamycin) pathway seems to play an important role in BC pathogenesis and it is possible to target this pathway by inhibitors such as rapamycin. In human BC cross talk between ER/PgR receptors signaling and the mTOR pathway is believed to be responsible for resistance to hormone therapy probably due to a down reg…

Cancer Researchmedicine.medical_specialtyCell growthmedicine.drug_classCancerBiologymedicine.diseaseEndocrinologyOncologyHormone receptorEstrogenInternal medicinemedicineCancer researchViability assayReceptorPI3K/AKT/mTOR pathwayTriple-negative breast cancerCancer Research
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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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Hypoxia-induced epithelial VEGF-C/VEGFR-3 upregulation in carcinoma cell lines

2008

Adaptation to hypoxia, a universal hallmark of carcinomas, is a critical step for tumor cell survival and growth. One of the principal regulators of hypoxia-responsive pathways is the transcription factor hypoxia-inducible factor-1 alpha (HIF-1 alpha). Currently, it is known that tumoral production of members of the vascular endothelial growth factor (VEGF)-family (VEGFs) may promote tumor growth and progression by acting on carcinoma cells that express the cognate receptors (VEGFRs). However, the influence of hypoxia in the formation of such a tumoral VEGF/VEGFR loop is not completely understood. In the present study we examined the potential existence of a HIF-1 alpha/VEGF/VEGFR autocrine…

Cancer Researchmedicine.medical_specialtyLung NeoplasmsVascular Endothelial Growth Factor CCellBreast NeoplasmsBiologychemistry.chemical_compoundDownregulation and upregulationCell Line TumorInternal medicinemedicineHumansAutocrine signallingVascular Endothelial Growth Factor Receptor-1CarcinomaKinase insert domain receptorCell cycleHypoxia-Inducible Factor 1 alpha SubunitVascular Endothelial Growth Factor Receptor-3Vascular Endothelial Growth Factor Receptor-2Cell HypoxiaUp-RegulationGene Expression Regulation NeoplasticVascular endothelial growth factorAutocrine CommunicationHIF1AEndocrinologymedicine.anatomical_structureOncologyVascular endothelial growth factor CchemistryCancer researchColorectal NeoplasmsInternational Journal of Oncology
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Transforming growth factor-β1, β2, and β3, urokinase and parathyroid hormone-related peptide expression in 8701-BC breast cancer cells and clones

1993

8701-BC is a recently characterized cell line isolated from a primary ductal infiltrating carcinoma of the breast (d.i.c.), showing some pleomorphism in cell microanatomy at an ultrastructural level. We have obtained different sublines of 8701-BC cells by cloning in soft agar at different concentrations (0.3% and 0.6%), and we have characterized the cloned lines by some morphological and growth parameters. 8701-BC cells and clones have been submitted to analysis by reverse transcriptase-linked polymerase chain reaction to detect mRNAs of various cytokines (transforming growth factor-beta s, tumour necrosis factors, interleukin 1s, interleukin 6, parathyroid hormone-related peptide, gamma in…

Cancer Researchmedicine.medical_specialtyMolecular Sequence DataParathyroid hormoneBreast NeoplasmsPolymerase Chain ReactionTransforming Growth Factor betaInternal medicineGene expressionBiomarkers TumorTumor Cells CulturedmedicineHumansRNA MessengerMolecular BiologyBase SequencebiologyParathyroid hormone-related proteinInterleukin-6Tumor Necrosis Factor-alphaCarcinoma Ductal BreastParathyroid Hormone-Related ProteinProteinsInterleukinCell BiologyTransforming growth factor betaUrokinase-Type Plasminogen ActivatorMolecular biologyIn vitroClone CellsPhenotypeEndocrinologyCell culturebiology.proteinInterleukin-1Developmental BiologyTransforming growth factorDifferentiation
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Physiological mechanisms regulating the expression of endothelial-type NO synthase

2002

Although endothelial nitric oxide synthase (eNOS) is a constitutively expressed enzyme, its expression is regulated by a number of biophysical, biochemical, and hormonal stimuli, both under physiological conditions and in pathology. This review summarizes the recent findings in this field. Shear stress, growth factors (such as transforming growth factor-beta, fibroblast growth factor, vascular endothelial growth factor, and platelet-derived growth factor), hormones (such as estrogens, insulin, angiotensin II, and endothelin 1), and other compounds (such as lysophosphatidylcholine) upregulate eNOS expression. On the other hand, the cytokine tumor necrosis factor-alpha and bacterial lipopolys…

Cancer Researchmedicine.medical_specialtyNitric Oxide Synthase Type IIIPhysiologyRNA Stabilitymedicine.medical_treatmentClinical BiochemistryBiologyFibroblast growth factorBiochemistryGene Expression Regulation Enzymologicchemistry.chemical_compoundEnosInternal medicinemedicineAnimalsPromoter Regions GeneticRegulation of gene expressionBase SequenceGene Expression ProfilingGrowth factorbiology.organism_classificationActin cytoskeletonAngiotensin IICell biologyVascular endothelial growth factorEndocrinologychemistryNitric Oxide SynthaseSignal transductionSignal TransductionNitric Oxide
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GADD45α is highly expressed in pancreatic ductal adenocarcinoma cells and required for tumor cell viability

2005

Pancreatic ductal adenocarcinoma is one of the most common causes of cancer death in the western civilization. Recently, NF-kappaB has been shown to be activated in pancreatic ductal adenocarcinoma through constitutive activation of IkappaB kinase (IKK). Inhibition of NF-kappaB by a super-inhibitor of NF-kappaB--delta-N-IkappaBalpha--resulted in impaired proliferation and induction of apoptosis, suggesting an important role of NF-kappaB in pancreatic tumorigenesis. Downstream target genes of IkappaBalpha have not been elucidated in pancreatic ductal adenocarcinoma in detail. Using expression profiling by cDNA array analysis of pancreatic ductal adenocarcinoma cell lines stably transfected w…

Cancer Researchmedicine.medical_specialtyPancreatic diseaseCell SurvivalDown-RegulationCell Cycle ProteinsIκB kinaseAdenocarcinomaBiologymedicine.disease_causeDownregulation and upregulationPancreatic cancerInternal medicinemedicineHumansCell ProliferationCell growthGene Expression ProfilingNF-kappa BNuclear Proteinsmedicine.diseaseI-kappa B KinasePancreatic NeoplasmsEndocrinologyOncologyApoptosisCancer researchRNA InterferenceCA19-9CarcinogenesisCarcinoma Pancreatic DuctalInternational Journal of Cancer
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Health status of young children with cancer following discontinuation of therapy.

1987

This paper reports late effects and health status of 198 children who had cancer or leukemia diagnosed under 2 years of age and their therapies electively withdrawn. This series (92 neuroblastoma (NBL), 57 Wilms' tumor (WT), 46 acute lymphoblastic leukemia (ALL), and 3 non-Hodgkin's lymphoma) was followed for 1-12 years after discontinuation of therapy. Thirty-three children were diagnosed before 1973, 92 between 1973 and 1977, and 73 after 1977 in 16 Italian Pediatric Oncology Centers. As of December 1983, 176 children were reported to be alive and without evidence of primary cancer by physicians responsible for their care. One child died from a second primary tumor, two from late recurren…

Cancer Researchmedicine.medical_specialtyPediatricsmedicine.medical_treatmentAntineoplastic AgentsGrowthNeoplasms Multiple PrimaryLeukoencephalopathyMuscular DiseasesNeoplasmsAcute lymphocytic leukemiamedicineHumansKyphoscoliosisChemotherapyRadiotherapybusiness.industryInfantCancerSequelamedicine.diseaseLeukemia LymphoidDiscontinuationSurgeryRadiation therapyOncologyChild PreschoolPediatrics Perinatology and Child HealthBone DiseasesNeoplasm Recurrence LocalNervous System DiseasesbusinessFollow-Up Studies
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