Search results for " protocols"

showing 10 items of 761 documents

Phase I Study of the Indoleamine 2,3-Dioxygenase 1 (IDO1) Inhibitor Navoximod (GDC-0919) Administered with PD-L1 Inhibitor (Atezolizumab) in Advanced…

2019

Abstract Purpose: IDO1 induces immune suppression in T cells through l-tryptophan (Trp) depletion and kynurenine (Kyn) accumulation in the local tumor microenvironment, suppressing effector T cells and hyperactivating regulatory T cells (Treg). Navoximod is an investigational small-molecule inhibitor of IDO1. This phase I study evaluated safety, tolerability, pharmacokinetics, and pharmacodynamics of navoximod in combination with atezolizumab, a PD-L1 inhibitor, in patients with advanced cancer. Patients and Methods: The study consisted of a 3+3 dose-escalation stage (n = 66) and a tumor-specific expansion stage (n = 92). Navoximod was given orally every 12 hours continuously for 21 consecu…

0301 basic medicineAdultCancer ResearchIndoles[SDV]Life Sciences [q-bio][SDV.BC]Life Sciences [q-bio]/Cellular BiologyPharmacologyAntibodies Monoclonal HumanizedArticleB7-H1 Antigen03 medical and health sciences0302 clinical medicinePharmacokineticsAtezolizumabRenal cell carcinomaNeoplasmsAntineoplastic Combined Chemotherapy ProtocolsmedicineBiomarkers TumorHumansIndoleamine-Pyrrole 23-DioxygenaseNeoplasm MetastasisAgedNeoplasm StagingAged 80 and overBladder cancerbusiness.industryMelanomaImidazolesMiddle Agedmedicine.diseaseMagnetic Resonance Imaging3. Good health030104 developmental biologyTreatment OutcomeOncologyTolerability030220 oncology & carcinogenesisPharmacodynamicsPD-L1 inhibitorbusinessTomography X-Ray Computed
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Adjuvant chemotherapy and relative survival of patients with stage II colon cancer - A EURECCA international comparison between the Netherlands, Denm…

2016

BACKGROUND: The aim of the present EURECCA international comparison is to compare adjuvant chemotherapy and relative survival of patients with stage II colon cancer between European countries.METHODS: Population-based national cohort data (2004-2009) from the Netherlands (NL), Denmark (DK), Sweden (SE), England (ENG), Ireland (IE), and Belgium (BE) were obtained, as well as single-centre data from Lithuania. All surgically treated patients with stage II colon cancer were included. The proportion of patients receiving adjuvant chemotherapy was calculated and compared between countries. Besides, relative survival was calculated and compared between countries.RESULTS: Overall, 59,154 patients …

0301 basic medicineAdultMaleCancer Researchmedicine.medical_specialtyAdjuvant chemotherapyColorectal cancerPopulationDiseasePopulation-basedStage II03 medical and health sciences0302 clinical medicinePharmacotherapySDG 3 - Good Health and Well-beingInternal medicineAntineoplastic Combined Chemotherapy ProtocolsJournal ArticlemedicineHumansStage (cooking)educationInternational comparisonAgedGynecologyeducation.field_of_studyRelative survivalbusiness.industryResearch Support Non-U.S. Gov'tMiddle Agedmedicine.diseaseSurvival AnalysisColon cancerAdjuvant chemotherapyEurope030104 developmental biologyLogistic ModelsOncologyChemotherapy Adjuvant030220 oncology & carcinogenesisColonic NeoplasmsSurgeryFemalebusinessStage ii colon cancerEuropean journal of cancer (Oxford, England : 1990)
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Impact of somatic mutations in myelodysplastic patients with isolated partial or total loss of chromosome 7

2020

Monosomy 7 [-7] and/or partial loss of chromosome 7 [del(7q)] are associated with poor and intermediate prognosis, respectively, in myelodysplastic syndromes (MDS), but somatic mutations may also play a key complementary role. We analyzed the impact on the outcomes of deep targeted mutational screening in 280 MDS patients with -7/del(7q) as isolated cytogenetic abnormality (86 with del(7q) and 194 with -7). Patients with del(7q) or -7 had similar demographic and disease-related characteristics. Somatic mutations were detected in 79% (93/117) of patients (82% in -7 and 73% in del(7q) group). Median number of mutations per patient was 2 (range 0-8). There was no difference in mutation frequen…

0301 basic medicineAdultMalemyelodysplastic syndromes chromosome abnormalities prognosisCancer Researchmedicine.medical_specialtyAdolescentSomatic cellTp53 mutationGastroenterology03 medical and health sciences0302 clinical medicinePartial lossCytogenetic AbnormalityInternal medicineAntineoplastic Combined Chemotherapy ProtocolsMedicineHumansMutation frequencyAgedChromosome 7 (human)Aged 80 and overbusiness.industryMyelodysplastic syndromesHematologyMiddle Agedmedicine.diseasePrognosisSurvival AnalysisMutational analysis030104 developmental biologyOncology030220 oncology & carcinogenesisMyelodysplastic SyndromesMutationFemaleChromosome DeletionbusinessChromosomes Human Pair 7
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FAST: a randomised phase II study of zolbetuximab (IMAB362) plus EOX versus EOX alone for first-line treatment of advanced CLDN18.2-positive gastric …

2021

Claudin 18.2 (CLDN18.2) is contained within normal gastric mucosa epithelial tight junctions; upon malignant transformation, CLDN18.2 epitopes become exposed. Zolbetuximab, a chimeric monoclonal antibody, mediates specific killing of CLDN18.2-positive cells through immune effector mechanisms.The FAST study enrolled advanced gastric/gastro-oesophageal junction and oesophageal adenocarcinoma patients (aged ≥18 years) with moderate-to-strong CLDN18.2 expression in ≥40% tumour cells. Patients received first-line epirubicin + oxaliplatin + capecitabine (EOX, arm 1, n = 84) every 3 weeks (Q3W), or zolbetuximab + EOX (loading dose, 800 mg/mIn the overall population, both PFS [hazard ratio (HR) = 0…

0301 basic medicineAdultmedicine.medical_specialtyAdolescentEsophageal NeoplasmsPopulationMedizinPhases of clinical researchAdenocarcinomaGastroenterologyLoading doseCapecitabine03 medical and health sciences0302 clinical medicineStomach NeoplasmsInternal medicineAntineoplastic Combined Chemotherapy ProtocolsmedicineClinical endpointHumanseducationCapecitabineeducation.field_of_studybusiness.industryHazard ratioAntibodies MonoclonalHematologyOxaliplatin030104 developmental biologyOncology030220 oncology & carcinogenesisClaudinsEsophagogastric Junctionbusinessmedicine.drugEpirubicinAnnals of oncology : official journal of the European Society for Medical Oncology
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5-year analysis of neoadjuvant pertuzumab and trastuzumab in patients with locally advanced, inflammatory, or early-stage HER2-positive breast cancer…

2016

Summary Background In the primary analysis of the NeoSphere trial, patients given neoadjuvant pertuzumab, trastuzumab, and docetaxel showed a significantly improved pathological complete response compared with those given trastuzumab and docetaxel after surgery. Here, we report 5-year progression-free survival, disease-free survival, and safety. Methods In this multicentre, open-label, phase 2 randomised trial in hospitals and medical clinics, treatment-naive adults with locally advanced, inflammatory, or early-stage HER2-positive breast cancer were randomly assigned (1:1:1:1) to receive four neoadjuvant cycles of trastuzumab (8 mg/kg loading dose, followed by 6 mg/kg every 3 weeks) plus do…

0301 basic medicineAdultmedicine.medical_specialtyTime FactorsAdolescentReceptor ErbB-2PopulationAntibodies Monoclonal HumanizedGastroenterologyGroup B03 medical and health sciencesYoung Adult0302 clinical medicineInternal medicineAntineoplastic Combined Chemotherapy ProtocolsmedicineHumanseducationSurvival rateAgedNeoplasm StagingAged 80 and overeducation.field_of_studybusiness.industryMiddle AgedTrastuzumabmedicine.diseasePrognosisNeoadjuvant TherapySurgerySurvival Rate030104 developmental biologyOncologyDocetaxelTolerabilityChemotherapy Adjuvant030220 oncology & carcinogenesisFemaleInflammatory Breast NeoplasmsPertuzumabNeoplasm Recurrence LocalbusinessFebrile neutropeniamedicine.drugEpirubicinFollow-Up StudiesThe Lancet. Oncology
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Pharmacogenetics of Metabolic Genes of Anthracyclines in Acute Myeloid Leukemia.

2018

Background Anthracyclines in combination with cytarabine have been the standard therapy for acute myeloid leukemia (AML) for decades with high efficacy. However, the majority of patients will show initial resistance or will relapse after initial complete remission. Genetic variability in genes involved in anthracyclines metabolic pathway could be one of the causes of the interindividual differences in clinical outcomes. Methods A systematic review of published studies in AML cohorts was carried out in order to analyze the influence of polymorphisms in genes of anthracycline metabolism on efficacy and toxicity. Results Polymorphisms in the main enzymes of anthracyclines metabolism (CBR, AKR,…

0301 basic medicineAnthracyclinemedicine.medical_treatmentClinical BiochemistryEfficacy03 medical and health sciences0302 clinical medicineAntineoplastic Combined Chemotherapy ProtocolsMedicineIdarubicinHumansAnthracyclinesPharmacologyCardiotoxicityChemotherapyPolymorphism Geneticbusiness.industryCytarabineMyeloid leukemiaLeukemia Myeloid Acute030104 developmental biologyPharmacogenetics030220 oncology & carcinogenesisCytarabineCancer researchbusinessPharmacogeneticsmedicine.drugCurrent drug metabolism
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Checkpoint Inhibition in Non-Hodgkin's Lymphoma.

2017

As patients continue to die from malignant lymphoma, novel treatment options continue to be warranted. To successfully grow and spread, tumor cells need to escape the immune system; therefore, the augmentation or restoration of immune effectors against the malignant cell could be of great value, as shown, e.g., for allogeneic transplantation. A deepened understanding of the regulation of activation and inhibition of the T cell-based effector mechanisms has led to the development of drugs that are able to modify specific checkpoints of this system and thereby raise an immune response against tumor cells. With dramatic responses observed in Hodgkin's disease (HD), interest has risen to explor…

0301 basic medicineCancer ResearchAllogeneic transplantationT cellT-LymphocytesAntineoplastic AgentsDisease03 medical and health sciences0302 clinical medicineImmune systemhemic and lymphatic diseasesAntineoplastic Combined Chemotherapy ProtocolsmedicineEffectorbusiness.industryLymphoma Non-HodgkinAntibodies MonoclonalHematologymedicine.diseaseIpilimumabLymphomaNon-Hodgkin's lymphoma030104 developmental biologymedicine.anatomical_structureNivolumabOncology030220 oncology & carcinogenesisCancer researchTumor EscapePrimary mediastinal B-cell lymphomabusinessRituximabOncology research and treatment
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9-ING-41, a small-molecule glycogen synthase kinase-3 inhibitor, is active in neuroblastoma.

2018

Advanced stage neuroblastoma is a very aggressive pediatric cancer with limited treatment options and a high mortality rate. Glycogen Synthase Kinase-3β (GSK-3β) is a potential therapeutic target in neuroblastoma. Using immunohistochemical staining, we observed positive GSK-3β expression in 67% of human neuroblastomas (34 out of 51 cases). Chemically distinct GSK-3 inhibitors (AR-A014418, TDZD8 and 9-ING-41), suppressed the growth of neuroblastoma cells whereas 9-ING-41, a clinically relevant small molecule GSK-3β inhibitor with broad spectrum pre-clinical antitumor activity, being the most potent. Inhibition of GSK-3 resulted in a decreased expression of the antiapoptotic molecule XIAP and…

0301 basic medicineCancer ResearchIndolesMice NudeCell Growth ProcessesIrinotecanArticleMaleimides03 medical and health sciencesMiceNeuroblastoma0302 clinical medicineGSK-3NeuroblastomaCell Line TumorAntineoplastic Combined Chemotherapy ProtocolsmedicineAnimalsHumansPharmacology (medical)Enzyme InhibitorsGlycogen synthasePharmacologyGlycogen Synthase Kinase 3 betabiologyChemistryDrug Synergismmedicine.diseasePediatric cancerXenograft Model Antitumor AssaysXIAP030104 developmental biologyOncologyCell cultureApoptosis030220 oncology & carcinogenesisCancer researchbiology.proteinImmunohistochemistryFemaleAnti-cancer drugs
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Tumor-Associated Fibroblasts Promote HER2-Targeted Therapy Resistance through FGFR2 Activation

2020

AbstractPurpose:Despite the therapeutic success of existing HER2-targeted therapies, tumors invariably relapse. This study aimed at identifying new mechanisms responsible for HER2-targeted therapy resistance.Experimental Design:We have used a platform of HER2-targeted therapy–resistant cell lines and primary cultures of healthy and tumor-associated fibroblasts (TAF) to identify new potential targets related to tumor escape from anti-HER2 therapies.Results:We have shown that TAFs promote resistance to HER2-targeted therapies. TAFs produce and secrete high levels of FGF5, which induces FGFR2 activation in the surrounding breast cancer cells. FGFR2 transactivates HER2 via c-Src, leading to res…

0301 basic medicineCancer ResearchReceptor ErbB-2medicine.medical_treatmentMice NudeBreast NeoplasmsDrug resistanceTargeted therapy03 medical and health sciencesMice0302 clinical medicineBreast cancerCancer-Associated FibroblastsTrastuzumabCell Line TumorAntineoplastic Combined Chemotherapy ProtocolsmedicineNeoplasmAnimalsHumansReceptor Fibroblast Growth Factor Type 2skin and connective tissue diseasesneoplasmsbusiness.industryLapatinibTrastuzumabmedicine.diseaseXenograft Model Antitumor AssaysSurvival Rate030104 developmental biologyOncologyTumor EscapeApoptosisDrug Resistance Neoplasm030220 oncology & carcinogenesisCancer researchFemaleSignal transductionNeoplasm Recurrence Localbusinessmedicine.drugSignal Transduction
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Tumor Microenvironment And Epithelial Mesenchymal Transition As Targets To Overcome Tumor Multidrug Resistance

2020

It is well established that multifactorial drug resistance hinders successful cancer treatment. Tumor cell interactions with the tumor microenvironment (TME) are crucial in epithelial-mesenchymal transition (EMT) and multidrug resistance (MDR). TME-induced factors secreted by cancer cells and cancer-associated fibroblasts (CAFs) create an inflammatory microenvironment by recruiting immune cells. CD11b+/Gr-1+ myeloid-derived suppressor cells (MDSCs) and inflammatory tumor associated macrophages (TAMs) are main immune cell types which further enhance chronic inflammation. Chronic inflammation nurtures tumor-initiating/cancer stem-like cells (CSCs), induces both EMT and MDR leading to tumor re…

0301 basic medicineCancer Researchmedicine.medical_treatmentMultidrug resistanceTargeted therapyTargeted therapy0302 clinical medicineCancer-Associated FibroblastsNeoplasmsAntineoplastic Combined Chemotherapy ProtocolsTumor-Associated MacrophagesTumor MicroenvironmentPharmacology (medical)HypoxiaTOR Serine-Threonine KinasesSmall moleculesChemotherapy ; Hypoxia ; Inflammation ; Microenvironment ; Multidrug resistance ; Small molecules ; Targeted therapy.Drug Resistance Multiple3. Good healthDNA DemethylationGene Expression Regulation NeoplasticInfectious DiseasesOncology030220 oncology & carcinogenesisInflammation MediatorsEpithelial-Mesenchymal TransitionStromal cellMicroenvironmentBiologyProinflammatory cytokine03 medical and health sciencesCell Line TumormedicineAnimalsHumansChemotherapyEpithelial–mesenchymal transitionPharmacologyInflammationTumor microenvironmentCancerHypoxia-Inducible Factor 1 alpha Subunitmedicine.diseaseHistone Deacetylase InhibitorsMultiple drug resistanceDisease Models Animal030104 developmental biologyDrug Resistance NeoplasmCancer cellCancer research
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