Search results for "antineoplastic"

showing 10 items of 2217 documents

FOLFIRINOX as induction treatment in rectal cancer patients with synchronous metastases: Results of the FFCD 1102 phase II trial

2018

Abstract Aim of the study The optimal therapeutic strategy in patients with rectal cancer and synchronous unresectable metastases remains unknown. We evaluated the efficacy of FOLFIRINOX induction therapy in this setting. Patients and methods Chemotherapy-naive patients received at least 8 cycles of FOLFIRINOX. The primary end-point was the 4-month disease control (4 m DC) rate. Tumour responses were centrally reviewed and assessed by computed tomography scan for metastases (Response Evaluation Criteria in Solid Tumours criteria) and magnetic resonance imaging for rectal tumorus. With a Simon 2-stage design and a targeted (H1) 4 m DC > 75%, 65 patients were enrolled from July 2012 to Februa…

MaleCancer ResearchLung NeoplasmsColorectal cancerFOLFIRINOXGastrointestinal DiseasesSynchronous metastasesLeucovorinKaplan-Meier EstimateInduction0302 clinical medicineInduction therapyAntineoplastic Combined Chemotherapy ProtocolsRectal cancerINDUCTION TREATMENTFatigueResponse rate (survey)medicine.diagnostic_testLiver NeoplasmsRemission InductionMiddle AgedCombined Modality TherapyMagnetic Resonance ImagingProgression-Free Survival3. Good healthOxaliplatinFOLFIRINOXTreatment OutcomeOncology030220 oncology & carcinogenesis030211 gastroenterology & hepatologyFemaleRadiologyFluorouracilAdultmedicine.medical_specialty[SDV.CAN]Life Sciences [q-bio]/CancerAdenocarcinomaIrinotecan03 medical and health sciencesmedicineHumansParesthesiaAgedPerformance statusbusiness.industryRectal NeoplasmsMagnetic resonance imagingmedicine.diseaseHematologic DiseasesConfidence intervalLocal controlbusinessTomography X-Ray ComputedFollow-Up Studies
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R-CVP versus R-CHOP versus R-FM for the initial treatment of patients with advanced-stage follicular lymphoma: results of the FOLL05 trial conducted …

2013

Purpose Although rituximab (R) is commonly used for patients with advanced follicular lymphoma (FL) requiring treatment, the optimal associated chemotherapy regimen has yet to be clarified. Patients and Methods We conducted an open-label, multicenter, randomized trial among adult patients with previously untreated stages II to IV FL to compare efficacy of eight doses of R associated with eight cycles of cyclophosphamide, vincristine, and prednisone (CVP) or six cycles of cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) or six cycles of fludarabine and mitoxantrone (FM). The principal end point of the study was time to treatment failure (TTF). Results There were 534 patients…

MaleCancer ResearchLymphomamedicine.medical_treatmentFollicular lymphomaCHOPGastroenterologyAntineoplastic Combined Chemotherapy ProtocolsProspective StudiesLymphoma FollicularNON-HODGKINS-LYMPHOMASAdult; Aged; Antineoplastic Combined Chemotherapy Protocols; Cyclophosphamide; Doxorubicin; Female; Follow-Up Studies; Humans; Lymphoma Follicular; Male; Middle Aged; Mitoxantrone; Neoplasm Grading; Neoplasm Staging; Prednisone; Prognosis; Prospective Studies; Survival Rate; Vidarabine; Vincristine; Oncology; Cancer ResearchCHEMOTHERAPYMiddle AgedPrognosisChemotherapy regimenFludarabineSurvival RateOncologyVincristineFemaleFLUDARABINECLINICAL-TRIALSVidarabinemedicine.drugAdultVincristinemedicine.medical_specialtyAdult; Aged; Antineoplastic Combined Chemotherapy Protocols; Cyclophosphamide; Doxorubicin; Female; Follow-Up Studies; Humans; Lymphoma Follicular; Male; Middle Aged; Mitoxantrone; Neoplasm Grading; Neoplasm Staging; Prednisone; Prognosis; Prospective Studies; Survival Rate; Vidarabine; VincristineInternal medicinemedicineHumansRITUXIMABSurvival rateCyclophosphamideRESPONSE CRITERIAAgedNeoplasm StagingChemotherapyMitoxantronebusiness.industryFollicularmedicine.diseasePHASE-IIISurgery1ST-LINE TREATMENTDoxorubicinPrednisoneMitoxantroneNeoplasm GradingbusinessFollow-Up StudiesJournal of clinical oncology : official journal of the American Society of Clinical Oncology
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Serum S100B levels correlate with clinical benefit in a metastatic melanoma patient treated by CTLA-4 blockade: a case report.

2013

<b><i>Background:</i></b> Cytotoxic T lymphocyte-associated antigen-4 (CTLA-4) is an immunoregulatory molecule expressed by activated T cells. In patients with metastatic melanoma, anti-CTLA-4 antibody therapy with ipilimumab achieves durable cancer regression in approximately 10-15% of patients. In the face of complex and sometimes delayed tumor response patterns, prognostic and predictive biomarkers are needed to monitor therapy outcomes and to identify early potential long-term survivors who might also benefit from therapy re-induction. <b><i>Case Report:</i></b> The clinical case of a 49-year-old male patient with metastatic melanoma and u…

MaleCancer ResearchMetastatic melanomamedicine.drug_classmedicine.medical_treatmentStatistics as TopicAntineoplastic AgentsS100 Calcium Binding Protein beta SubunitMonoclonal antibodySensitivity and SpecificitymedicineBiomarkers TumorCytotoxic T cellHumansCTLA-4 AntigenMelanomabusiness.industryMelanomaAntibodies MonoclonalReproducibility of ResultsHematologyImmunotherapyMiddle Agedmedicine.diseaseIpilimumabBlockadeTreatment OutcomeOncologyCTLA-4Cancer researchBiomarker (medicine)businessOnkologie
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Inhibition of DNA methylation sensitizes glioblastoma for tumor necrosis factor-related apoptosis-inducing ligand-mediated destruction.

2005

AbstractLife expectancy of patients affected by glioblastoma multiforme is extremely low. The therapeutic use of tumor necrosis factor–related apoptosis-inducing ligand (TRAIL) has been proposed to treat this disease based on its ability to kill glioma cell lines in vitro and in vivo. Here, we show that, differently from glioma cell lines, glioblastoma multiforme tumors were resistant to TRAIL stimulation because they expressed low levels of caspase-8 and high levels of the death receptor inhibitor PED/PEA-15. Inhibition of methyltransferases by decitabine resulted in considerable up-regulation of TRAIL receptor-1 and caspase-8, down-regulation of PED/PEA-15, inhibition of cell growth, and …

MaleCancer ResearchMethyltransferaseNudeDrug ResistanceApoptosisReceptors Tumor Necrosis FactorTNF-Related Apoptosis-Inducing LigandCASPASE-8 EXPRESSIONMiceNude mouseSIGNALING COMPLEXReceptorsAntineoplastic Combined Chemotherapy ProtocolsTumor Cells CulturedDNA Modification MethylasesIN-VIVOHeterologousCaspase 8CulturedMembrane GlycoproteinsbiologyIntracellular Signaling Peptides and ProteinsMiddle AgedTumor CellsGene Expression Regulation NeoplasticMALIGNANT GLIOMA-CELLSOncologyCaspasesDNA methylationAzacitidineTumor necrosis factor alphaFemalemedicine.drugSignal TransductionAdultBRAIN-TUMORSTransplantation HeterologousCHEMOTHERAPEUTIC-AGENTSDecitabineMice NudeDecitabineDRUG-INDUCED APOPTOSISDEATH RECEPTOR5-AZA-2'-DEOXYCYTIDINEIn vivoSettore MED/04 - PATOLOGIA GENERALEmedicineAnimalsHumansneoplasmsAgedTransplantationNeoplasticCell growthTumor Necrosis Factor-alphaHistocompatibility Antigens Class IDNA Methylationbiology.organism_classificationPhosphoproteinsReceptors TNF-Related Apoptosis-Inducing LigandGene Expression RegulationApoptosisDrug Resistance NeoplasmImmunologyCancer researchNeoplasmAdult; Aged; Animals; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Apoptosis Regulatory Proteins; Azacitidine; Caspase 8; Caspases; DNA Modification Methylases; Drug Resistance Neoplasm; Female; Glioblastoma; Histocompatibility Antigens Class I; Humans; Intracellular Signaling Peptides and Proteins; Male; Membrane Glycoproteins; Mice; Mice Nude; Middle Aged; Phosphoproteins; Receptors TNF-Related Apoptosis-Inducing Ligand; Receptors Tumor Necrosis Factor; Signal Transduction; TNF-Related Apoptosis-Inducing Ligand; Transplantation Heterologous; Tumor Cells Cultured; Tumor Necrosis Factor-alpha; DNA Methylation; Gene Expression Regulation Neoplastic; Cancer Research; OncologyTumor Necrosis FactorTRAIL-INDUCED APOPTOSISApoptosis Regulatory ProteinsGlioblastomaCancer research
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Synergistic Antioncogenic Activity of Azacitidine and Curcumin in Myeloid Leukemia Cell Lines and Patient Samples.

2019

Background/aim Azacitidine (AZA) is a hypomethylating agent used in myeloid neoplasms, however, approximately half of patients show treatment failure or relapse. This in vitro study investigated the effect of the combination of AZA with the natural compound curcumin (CUR) in increasing its efficacy. Materials and methods We analyzed the effects of AZA plus CUR on proliferation, apoptosis, cell cycle and differentiation in myeloid leukemic cell lines (U-937, HL-60, K-562, and OCI-AML3) and bone marrow samples of patients. Results The results showed a synergy between AZA and CUR in all leukemic lines and in most leukemic samples, with a decrease in proliferation and an increase in apoptosis c…

MaleCancer ResearchMyeloidCurcuminAzacitidineAntineoplastic AgentsApoptosis03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCell Line TumormedicineHumansAgedAged 80 and overbusiness.industryCell CycleMyeloid leukemiaCell DifferentiationDrug SynergismGeneral MedicineCell cyclemedicine.anatomical_structureOncologychemistryHypomethylating agentApoptosisLeukemia Myeloid030220 oncology & carcinogenesisMyelodysplastic SyndromesCancer researchCurcuminAzacitidineFemaleBone marrowbusinessmedicine.drugAnticancer research
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Second primary malignancies in patients treated for gastric mucosa-associated lymphoid tissue lymphoma.

2017

IF 2.755; International audience; To assess the risk of second primary malignancy (SPM) in patients with gastric mucosa-associated lymphoid tissue (MALT) Lymphoma (GML), we included 175 patients with GML in the present study. The incidence of SPM in the general population, used for reference, was determined from the French network of cancer registries. During the 1442.9 patient-years of follow-up, 29 patients were diagnosed with incident SPM, including five patients diagnosed with gastric cancer (20.1/1000 patient-years). An increased incidence of SPM was observed in patients with GML (standardized incidence ratios [SIR]: 1.71 [1.14-2.45]) compared to the general French population especiall…

MaleCancer ResearchPathologymedicine.medical_treatmentGastroenterology[ SDV.CAN ] Life Sciences [q-bio]/CancerMALT0302 clinical medicinerituximabAntineoplastic Combined Chemotherapy Protocolsalkylating agentsAged 80 and overeducation.field_of_studyrituximab plus chlorambucilbiologyIncidence (epidemiology)Incidencet(11.18) translocationNeoplasms Second PrimaryHematologyMiddle Aged3. Good healthmedicine.anatomical_structureOncology030220 oncology & carcinogenesis030211 gastroenterology & hepatologyFemaleImmunotherapymedicine.medical_specialtyPopulation[SDV.CAN]Life Sciences [q-bio]/CancerMalignancy03 medical and health sciencesStomach NeoplasmsInternal medicinemedicineGastric mucosaHumanseducationAgedNeoplasm StagingRetrospective StudiesChemotherapyRadiotherapybusiness.industryfungiCancerLymphoma B-Cell Marginal ZoneHelicobacter pylorimedicine.diseasebiology.organism_classificationLymphomaOriginal Article: ClinicalbusinessFollow-Up Studies
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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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