Search results for "Neoplastic"

showing 10 items of 2901 documents

Pyrrolotetrazinones deazaanalogues of temozolomide induce apoptosis in Jurkat cell line: involvement of tubulin polymerization inhibition.

2009

Pyrrolotetrazinones are a new class of azolotetrazinones endowed with a high, remarkable antiproliferative activity in human tumor cultured cells. They hold the deaza skeleton of the antitumor drug temozolomide, although preliminary investigations indicated a different mechanism of action. To understand their mechanism(s) of action along with their target at molecular level, four derivatives were selected on the basis of their activity on a panel of human tumor cell lines and they were investigated in depth in a T leukemia cell line (Jurkat). Flow cytometric analysis of cell cycle after treatment with pyrrolotetrazinones has demonstrated that they were able to induce an arrest of the cell c…

MaleCancer ResearchProgrammed cell deathCarcinoma HepatocellularCell SurvivalCellGene ExpressionAntineoplastic AgentsApoptosisPhosphatidylserinesBiologyToxicologyJurkat cellsMicrotubulesMicrotubule polymerizationJurkat CellsMiceTubulinCell Line TumormedicineTemozolomideAnimalsHumansPharmacology (medical)Cell Proliferationbcl-2-Associated X ProteinPharmacologyMembrane Potential MitochondrialMice Inbred BALB CCaspase 3Cell CycleCell MembraneCell cycleSettore CHIM/08 - Chimica FarmaceuticaTubulin ModulatorsCell biologyMitochondriaDacarbazinemedicine.anatomical_structureOncologyMechanism of actionBiochemistryProto-Oncogene Proteins c-bcl-2ApoptosisCell culturemedicine.symptomPoly(ADP-ribose) PolymerasesReactive Oxygen SpeciesPyrrolotetrazinoneCancer chemotherapy and pharmacology
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cAMP-dependent phosphorylation of CYP2B1 as a functional switch for cyclophosphamide activation and its hormonal controlin vitro andin vivo

2001

An important feature of cytochrome P450 (CYP) 2B1 is its high ability to convert the prodrug cyclophosphamide (CPA) to therapeutically cytotoxic metabolites, resulting in interstrand DNA-cross-linking and cell death. We have examined whether and how the phosphorylation of CYP2B1 influences CPA metabolic activation in vitro and in vivo. We found first that only part of the total CYP2B1 pool undergoes phosphorylation. This part is fully inactivated. Second, phosphorylation of CYP2B1 in intact hepatocytes reduced by up to 75% toxification of CPA to mutagenic metabolites (totally dependent on the same preferentially CYP2B-catalyzed 4-hydroxylation of CPA as is the generation of highly cytotoxic…

MaleCancer ResearchProgrammed cell deathTime FactorsCellRats Sprague-DawleyStructure-Activity RelationshipSex FactorsIn vivoCyclic AMPPhosphoprotein PhosphatasesSerinemedicineAnimalsCytotoxic T cellheterocyclic compoundsPhosphorylationProtein kinase AAntineoplastic Agents AlkylatingCyclophosphamideBiotransformationbiologyCytochrome P450GlucagonCyclic AMP-Dependent Protein KinasesIn vitroRatsCell biologymedicine.anatomical_structureOncologyBiochemistryCytochrome P-450 CYP2B1Hepatocytescardiovascular systembiology.proteinPhosphorylationFemaleMutagensInternational Journal of Cancer
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Early Skin Toxicity as a Predictive Factor for Tumor Control in Hepatocellular Carcinoma Patients Treated with Sorafenib.

2010

Abstract Introduction. Sorafenib is an oral multikinase inhibitor that targets Raf kinase and receptor tyrosine kinases and has led to a longer median overall survival (OS) time and time to progression (TTP) in patients with advanced hepatocellular carcinoma (HCC). This study was conducted to assess the link between the antitumor efficacy of sorafenib and its early cutaneous side effects in advanced HCC patients. Materials and Methods. All patients received 800 mg daily of sorafenib until progression or unacceptable toxicities. We retrospectively analyzed the incidence of rash and hand–foot skin reactions (HFSR) during the first month of treatment, comparing tumor control (partial response …

MaleCancer ResearchPyridinesSettore MED/06 - Oncologia MedicaKaplan-Meier EstimateGastroenterologySkin Toxicity Hepatocellular CarcinomaSorafenib.Aged 80 and overintegumentary systemIncidence (epidemiology)BenzenesulfonatesLiver NeoplasmsMiddle AgedSorafenibRashhumanitiesOncologyHepatocellular carcinomaToxicityDisease ProgressionFemaleDrug Eruptionsmedicine.symptommedicine.drugAdultNiacinamideSorafenibmedicine.medical_specialtyCarcinoma HepatocellularAntineoplastic AgentsInternal medicinemedicineCarcinomaHumansneoplasmsSurvival analysisAgedRetrospective StudiesSurrogate endpointbusiness.industryPhenylurea CompoundsExanthemamedicine.diseaseSurvival Analysisdigestive system diseasesSurgerybody regionsMultivariate AnalysisHepatobiliarybusiness
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Trastuzumab therapy vs tetracycline controlled ERBB2 downregulation: influence on tumour development in an ERBB2-dependent mouse tumour model

2008

Trastuzumab (Herceptin) has improved therapy of breast cancer. Only patients overexpressing ERBB2 are treated with trastuzumab, whereas its use in tumours without ERBB2 expression is useless. This led to the concept that the subgroup of trastuzumab-sensitive tumours is ‘ERBB2-dependent', meaning that ERBB2 signalling is indispensable for growth of these tumours. We used a mouse model that allows anhydrotetracycline (ATc)-controlled downregulation of ERBB2 in tumour tissue. ERBB2 mRNA and protein expression were downregulated below detection limit leading to a macroscopically complete tumour remission within 14 days. Tumour remission was accompanied by a strong decrease in proliferation, a m…

MaleCancer ResearchReceptor ErbB-2AKT1AKT2ApoptosisMiceTrastuzumabPKBskin and connective tissue diseasesERBB2Mitogen-Activated Protein Kinase 3biologyERK1/2herceptinAntibodies MonoclonalCytochromes cImmunohistochemistrynude miceGene Expression Regulation NeoplasticOncologyTetracyclinesKi-67Ki-67Femalemedicine.drugmedicine.medical_specialtyBlotting WesternDown-RegulationMice NudeAntineoplastic AgentsProtein Serine-Threonine KinasesAntibodies Monoclonal Humanizedresistance3-Phosphoinositide-Dependent Protein Kinasesbreast cancerDownregulation and upregulationresponse to therapyInternal medicineHER2medicineAnimalsRNA Messengercytochrome c releaseProtein kinase Bneoplasmstumour developmentCell Proliferationhumanised monoclonal antibodyAktCancerMammary Neoplasms ExperimentalTrastuzumabmedicine.diseaseEndocrinologyKi-67 AntigenApoptosisDrug Resistance Neoplasmbiology.proteinCancer researchreceptor tyrosine kinaseTranslational TherapeuticsProto-Oncogene Proteins c-aktBritish Journal of Cancer
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Analysis of t(15;17) chromosomal breakpoint sequences in therapy-related versus de novo acute promyelocytic leukemia: Association of DNA breaks with …

2010

We compared genomic breakpoints at the PML and RARA loci in 23 patients with therapy-related acute promyelocytic leukemia (t-APL) and 25 de novo APL cases.Eighteen of 23 t-APL cases received the topoisomerase II poison mitoxantrone for their primary disorder. DNA breaks were clustered in a previously reported 8 bp "hot spot" region of PML corresponding to a preferred site of mitoxantrone-induced DNA topoisomerase II-mediated cleavage in 39% of t-APL occurring in patients exposed to this agent and in none of the cases arising de novo (P = 0.007). As to RARA breakpoints, clustering in a 3' region of intron 2 (region B) was found in 65% of t-APL and 28% of de novo APL patients, respectively. S…

MaleCancer ResearchReceptors Retinoic AcidRetinoic AcidMessengerPromyelocytic Leukemia ProteinTranslocation GeneticChromosome BreakpointsLeukemia Promyelocytic Acuteimmune system diseasesReceptorsPromyelocyticGeneticsLeukemiabiologyReverse Transcriptase Polymerase Chain ReactionRetinoic Acid Receptor alphaNuclear ProteinsDNA NeoplasmMiddle AgedFemaleHumanAdultAcute promyelocytic leukemiaChromosome BreakpointsTranslocationAntineoplastic AgentsAcuteChromosomesYoung AdultPromyelocytic leukemia proteinGeneticGeneticsmedicineConsensus sequenceHumansRNA MessengerReceptors Retinoic Acid; Male; Young Adult; Middle Aged; Chromosome Breakpoints; Female; Chromosomes Human Pair 17; Tumor Suppressor Proteins; Humans; DNA Neoplasm; Translocation Genetic; Leukemia Promyelocytic Acute; Antineoplastic Agents; Nuclear Proteins; RNA Messenger; Mitoxantrone; Reverse Transcriptase Polymerase Chain Reaction; Chromosomes Human Pair 15; Transcription Factors; Aged; AdultneoplasmsAgedChromosomes Human Pair 15Pair 17Tumor Suppressor ProteinsTopoisomeraseBreakpointPair 15DNAmedicine.diseaseRetinoic acid receptor alphabiology.proteinNeoplasmRNAHuman genomeMitoxantroneSettore MED/15 - Malattie del SangueChromosomes Human Pair 17Transcription FactorsGenes, Chromosomes and Cancer
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Prostate cancer: from the pathophysiologic implications of some genetic risk factors to translation in personalized cancer treatments.

2013

Several pathologies affect human prostate, such as prostate cancer (PC), which is the most common non-skin malignant cancer in Western male populations. A complex interaction between genetic and environmental factors (i.e. infectious agents, dietary carcinogens) and hormonal imbalances has been reported to have a fundamental role in PC pathophysiology by evoking chronic inflammation. Thus, chronic inflammation drives prostate carcinogenesis and neoplastic progression. No adequate biomarkers exist until now to guide PC prognosis and treatment. Accordingly, the research has particularly focused its attention on genetic variants in genes, codifying molecules of signaling innate immune/inflamma…

MaleCancer ResearchSNPBioinformaticsTranslational Research BiomedicalProstate cancersex steroid and inflammatory networkRisk FactorsmedicineSettore MED/05 - Patologia ClinicaHumansGenetic Predisposition to DiseaseGenetic riskPrecision MedicineGonadal Steroid HormonesMolecular BiologyAllelesSettore MED/04 - Patologia GeneraleInflammationPolymorphism Geneticbusiness.industryrisk profileCancerProstatic NeoplasmsTranslation (biology)prostate cancermedicine.diseasePathophysiologypersonalized PC medicineCell Transformation NeoplasticImmunologygenetic biomarkerDisease ProgressionMolecular MedicinebusinessSignal TransductionCancer gene therapy
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Oxidative stress in bisphosphonate-related osteonecrosis of the jaws

2013

Objectives To analyze whether oxidative stress (OS) changes are present in patients with bisphosphonate-related osteonecrosis of the jaw (BRONJ) versus controls. Materials and Methods Oxidative stress was analyzed in serum and unstimulated saliva of three groups: Group 1 consisted of 24 patients who had been treated with intravenous bisphosphonates (ivBPs) and developed BRONJ, group 2 consisted of 20 patients who had received ivBPs and did not develop BRONJ, and group 3 comprised 17 control subjects. Reduced glutathione (GSH), malondialdehyde (MDA), oxidized glutathione (GSSG), and 8–oxo-7,8-dihydro-2-deoxyguanosine (8-oxo-dG) levels, as well as the GSSG/GSH ratio, were measured. Results Me…

MaleCancer ResearchSalivaOral Hygiene Indexmedicine.medical_treatmentmedicine.disease_causeGastroenterologychemistry.chemical_compoundfluids and secretionsAdrenal Cortex HormonesMalondialdehydeDiphosphonatesGlutathione DisulfideDental Plaque IndexMiddle AgedMalondialdehydeGlutathione8-Hydroxy-2'-DeoxyguanosinePeriodonticsAdministration IntravenousBisphosphonate-Associated Osteonecrosis of the JawFemaleOral SurgeryMultiple Myelomamedicine.medical_specialtyAntineoplastic AgentsBreast NeoplasmsPathology and Forensic MedicineSex FactorsInternal medicinemedicineHumansSalivaAgedBisphosphonate-associated osteonecrosis of the jawDMF Indexbusiness.industryDeoxyguanosineGlutathioneBisphosphonatemedicine.diseaseSurgeryOxidative StressOtorhinolaryngologychemistryCase-Control StudiesGlutathione disulfideOsteonecrosis of the jawbusinessBiomarkersOxidative stressJournal of Oral Pathology & Medicine
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Complete tumor prevention by engineered tumor cell vaccines employing nonviral vectors.

2004

We report that 100% mice survival after tumor challenge is achieved with cytokine-engineered cells employing nonviral lipoplexes and without using viral vectors. We describe this effect with cytokine-secreting tumor cell vaccines, based on cell clones or fresh transfected cells. Tumor cells were transfected with murine granulocyte-macrophage colony-stimulating factor (GM-CSF) or IL-4 plasmids employing the cationic lipid DOTAP, were irradiated (150 Gy) and kept frozen until use. The transfection efficacy was analyzed by qRT-PCR and flow cytometry. Vaccination induced potent antitumor rejection, resulting in 100% mice survival. Furthermore, the antitumor immunity was long lasting, since a tw…

MaleCancer ResearchSkin NeoplasmsGenetic enhancementCellGenetic VectorsAntineoplastic AgentsBiologyCancer VaccinesViral vectorFlow cytometryMicemedicineAnimalsMolecular BiologyMelanomaInterleukin 4medicine.diagnostic_testReverse Transcriptase Polymerase Chain ReactionMelanomaGranulocyte-Macrophage Colony-Stimulating FactorTransfectionGenetic TherapyNeoplasms Experimentalmedicine.diseaseFlow CytometryVirologySurvival AnalysisMice Inbred C57BLmedicine.anatomical_structureGranulocyte macrophage colony-stimulating factorMolecular MedicineFemaleInterleukin-4Genetic Engineeringmedicine.drugCancer gene therapy
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ERGO: A pilot study of ketogenic diet in recurrent glioblastoma

2014

Limiting dietary carbohydrates inhibits glioma growth in preclinical models. Therefore, the ERGO trial (NCT00575146) examined feasibility of a ketogenic diet in 20 patients with recurrent glioblastoma. Patients were put on a low-carbohydrate, ketogenic diet containing plant oils. Feasibility was the primary endpoint, secondary endpoints included the percentage of patients reaching urinary ketosis, progression-free survival (PFS) and overall survival. The effects of a ketogenic diet alone or in combination with bevacizumab was also explored in an orthotopic U87MG glioblastoma model in nude mice. Three patients (15%) discontinued the diet for poor tolerability. No serious adverse events attri…

MaleCancer ResearchStatement (logic)medicine.medical_treatmentSalvage treatmentPilot ProjectsBioinformaticsGastroenterologyMicegliomaClinical endpoint1306 Cancer ResearchglucoseArticlesMiddle AgedCombined Modality TherapyBevacizumabTreatment OutcomeTolerabilityOncologyketogenic dietFemale2730 OncologyDiet Ketogenicmedicine.drugAdultmedicine.medical_specialtyBevacizumabMice NudeAntineoplastic Agents610 Medicine & healthMistakeRecurrent GliomaBiologyAntibodies Monoclonal HumanizedInternal medicineGliomamedicineAnimalsHumansddc:610Adverse effectAgedbusiness.industryRecurrent glioblastomaGeneral surgeryKetosisNeoplasms Experimentalmedicine.diseaseSurvival Analysis10040 Clinic for NeurologySurgeryQuality of LifeNeoplasm Recurrence LocalKetosisGlioblastomabusinessmetabolismfeasibilityKetogenic dietInternational Journal of Oncology
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Castration-Induced Downregulation of SPARC in Stromal Cells Drives Neuroendocrine Differentiation of Prostate Cancer.

2021

Abstract Fatal neuroendocrine differentiation (NED) of castration-resistant prostate cancer is a recurrent mechanism of resistance to androgen deprivation therapies (ADT) and antiandrogen receptor pathway inhibitors (ARPI) in patients. The design of effective therapies for neuroendocrine prostate cancer (NEPC) is complicated by limited knowledge of the molecular mechanisms governing NED. The paucity of acquired genomic alterations and the deregulation of epigenetic and transcription factors suggest a potential contribution from the microenvironment. In this context, whether ADT/ARPI induces stromal cells to release NED-promoting molecules and the underlying molecular networks are unestablis…

MaleCancer ResearchStromal cellAnimals Biomarkers Tumor Cell Differentiation Cell Line Tumor Coculture Techniques Endoplasmic Reticulum Chaperone BiP Epigenesis Genetic Gene Expression Regulation Neoplastic Humans Male Mice Mice Inbred C57BL Neuroendocrine Cells Osteonectin Prostatic Neoplasms Stromal Cells Transgenes Tumor Microenvironment Down-RegulationDown-RegulationContext (language use)Settore MED/08 - Anatomia PatologicaNeuroendocrine differentiationEpigenesis GeneticProstate cancerMiceStromaDownregulation and upregulationNeuroendocrine CellsCell Line TumormedicineBiomarkers TumorTumor MicroenvironmentSettore MED/05 - Patologia ClinicaAnimalsHumansOsteonectinEpigeneticsTransgenesEndoplasmic Reticulum Chaperone BiPbusiness.industryMatricellular proteinProstatic NeoplasmsCell Differentiationmedicine.diseaseCoculture TechniquesGene Expression Regulation NeoplasticMice Inbred C57BLOncologyCancer researchStromal CellsbusinessCancer research
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