Search results for "vemurafenib"

showing 10 items of 22 documents

Clinical outcome of concomitant vs interrupted BRAF inhibitor therapy during radiotherapy in melanoma patients

2018

Background: Concomitant radiation with BRAF inhibitor (BRAFi) therapy may increase radiation-induced side effects but also potentially improve tumour control in melanoma patients. Methods: A total of 155 patients with BRAF-mutated melanoma from 17 European skin cancer centres were retrospectively analysed. Out of these, 87 patients received concomitant radiotherapy and BRAFi (59 vemurafenib, 28 dabrafenib), while in 68 patients BRAFi therapy was interrupted during radiation (51 vemurafenib, 17 dabrafenib). Overall survival was calculated from the first radiation (OSRT) and from start of BRAFi therapy (OSBRAFi). Results: The median duration of BRAFi treatment interruption prior to radiothera…

0301 basic medicineOncologyMaleCancer ResearchRadiation-Sensitizing AgentsSkin Neoplasmsmedicine.medical_treatmentMedizinCohort Studies0302 clinical medicineAntineoplastic Combined Chemotherapy ProtocolsOximesVemurafenibProspective cohort studyMelanomaAged 80 and overMelanomaImidazolesMiddle AgedTreatment OutcomeOncology030220 oncology & carcinogenesisFemalemedicine.drugAdultProto-Oncogene Proteins B-rafmedicine.medical_specialtyAdolescentDrug Administration ScheduleBRAF03 medical and health sciencesYoung AdultInternal medicinemedicineHumansddc:610dabrafenibProtein Kinase InhibitorsradiotherapyAgedRetrospective Studiesbusiness.industryDabrafenibRetrospective cohort studymedicine.diseaseRadiation therapyradiation030104 developmental biologyVemurafenibConcomitantClinical StudySkin cancerbusinessBritish Journal of Cancer
researchProduct

Progression patterns under BRAF inhibitor treatment and treatment beyond progression in patients with metastatic melanoma

2017

Despite markedly improved treatment options for metastatic melanoma, resistance to targeted therapies such as BRAF inhibitors (BRAFi) or BRAFi plus MEK inhibitors (MEKi) remains a major problem. Our aim was to characterize progression on BRAFi therapy and outcome of subsequent treatment. One hundred and eighty patients with BRAF-mutant metastatic melanoma who had progressed on treatment with single-agent BRAFi from February 2010 to April 2015 were included in a retrospective data analysis focused on patterns of progression, treatment beyond progression (TBP) and subsequent treatments after BRAFi therapy. Analysis revealed that 51.1% of patients progressed with both new and existing metastas…

0301 basic medicineOncologyMaleCancer ResearchSkin NeoplasmsBRAF inhibitorProgrammed Cell Death 1 ReceptorMedizinKaplan-Meier Estimate0302 clinical medicineAntineoplastic Combined Chemotherapy ProtocolsVemurafenibMelanomaOriginal ResearchAged 80 and overTreatment optionsMiddle AgedMAP Kinase Kinase KinasesPrognosisProgression-Free SurvivalOncology030220 oncology & carcinogenesisDisease ProgressionvemurafenibFemalemedicine.drugmetastatic melanomaBRAF inhibitorAdultProto-Oncogene Proteins B-rafmedicine.medical_specialtyMetastatic melanomaRetrospective data03 medical and health sciencesYoung AdultInternal medicinetreatment beyond progressionmedicineOverall survivalHumansRadiology Nuclear Medicine and imagingIn patientdabrafenibProtein Kinase InhibitorsResponse Evaluation Criteria in Solid TumorsAgedRetrospective Studiesbusiness.industryClinical Cancer ResearchDabrafenib030104 developmental biologyBRAF mutationDrug Resistance NeoplasmMutationprogressionbusinessFollow-Up StudiesCancer Medicine
researchProduct

Update on tolerability and overall survival in COLUMBUS: landmark analysis of a randomised phase 3 trial of encorafenib plus binimetinib vs vemurafen…

2020

Abstract Background BRAF/MEK inhibitor combinations are established treatments for BRAF V600–mutant melanoma based on demonstrated benefits on progression-free survival (PFS) and overall survival (OS). Here, we report an updated analysis of the COLUMBUS (COmbined LGX818 [encorafenib] Used with MEK162 [binimetinib] in BRAF mutant Unresectable Skin cancer) trial with long-term follow-up. Methods In part 1 of the COLUMBUS trial, 577 patients with advanced/metastatic BRAF V600–mutant melanoma, untreated or progressed after first-line immunotherapy, were randomised 1:1:1 to 450 mg of encorafenib QD + 45 mg of binimetinib BID (COMBO450) vs 960 mg of vemurafenib BID (VEM) or 300 mg of encorafenib …

0301 basic medicineOncologyMaleCancer ResearchSkin NeoplasmsMedizinchemistry.chemical_compound0302 clinical medicineAntineoplastic Combined Chemotherapy ProtocolsOutcome Assessment Health CareMedicine1306 Cancer ResearchVemurafenibMelanomaAged 80 and overSulfonamidesMEK inhibitorMelanomaHazard ratio10177 Dermatology ClinicBinimetinibNauseaMiddle AgedPrognosisOncologyTolerability030220 oncology & carcinogenesis2730 OncologyFemalemedicine.drugAdultDiarrheaProto-Oncogene Proteins B-rafmedicine.medical_specialtyVomiting610 Medicine & healthDisease-Free Survival03 medical and health sciencesInternal medicineHumansneoplasmsAgedbusiness.industrymedicine.diseaseConfidence interval030104 developmental biologychemistryVemurafenibMutationBenzimidazolesCarbamatesSkin cancerbusinessEuropean journal of cancer (Oxford, England : 1990)
researchProduct

BRAF as a positive predictive biomarker: Focus on lung cancer and melanoma patients

2020

In the era of personalized medicine, BRAF mutational assessment is mandatory in advanced-stage melanoma and non-small cell lung cancer (NSCLC) patients. The identification of actionable mutations is crucial for the adequate management of these patients. To date various drugs have been implemented in clinical practice. Similarly, various methods may be adopted for the identification of BRAF mutations. Here, we briefly review the current literature on BRAF in melanoma and NSCLC, focusing attention in particular on the different methods and drugs adopted in these patients. In addition, an overview of the real-world practice in different Italian laboratories with high expertise in molecular pre…

0301 basic medicineOncologyProto-Oncogene Proteins B-rafmedicine.medical_specialtyPredictive molecular pathologyLung NeoplasmsGene mutationBRAF03 medical and health scienceschemistry.chemical_compound0302 clinical medicineInternal medicineCarcinoma Non-Small-Cell LungMedicineHumansNon-Small-Cell LungVemurafenibLung cancerneoplasmsMelanomaTrametinibCobimetinibbusiness.industryBRAF; Lung cancer; Melanoma; Precision medicine; Predictive molecular pathology; Biomarkers; Humans; Mutation; Proto-Oncogene Proteins B-raf; Carcinoma Non-Small-Cell Lung; Lung Neoplasms; MelanomaCarcinomaPrecision medicineDabrafenibHematologyBiomarkerPrecision medicinemedicine.diseaseBRAF; Lung cancer; Melanoma; Precision medicine; Predictive molecular pathologyLung Neoplasm030104 developmental biologyOncologychemistry030220 oncology & carcinogenesisMutationPersonalized medicineLung cancerbusinessBiomarkersmedicine.drugHuman
researchProduct

Encorafenib plus binimetinib versus vemurafenib or encorafenib in patients with BRAF -mutant melanoma (COLUMBUS): a multicentre, open-label, randomis…

2017

Summary Background Combined BRAF-MEK inhibitor therapy is the standard of care for BRAF V600 -mutant advanced melanoma. We investigated encorafenib, a BRAF inhibitor with unique target-binding properties, alone or in combination with the MEK inhibitor binimetinib, versus vemurafenib in patients with advanced BRAF V600 -mutant melanoma. Methods COLUMBUS was conducted as a two-part, randomised, open-label phase 3 study at 162 hospitals in 28 countries. Eligible patients were aged 18 years or older and had histologically confirmed locally advanced (American Joint Committee on Cancer [AJCC] stage IIIB, IIIC, or IV), unresectable or metastatic cutaneous melanoma, or unknown primary melanoma; a B…

AdultMaleProto-Oncogene Proteins B-raf0301 basic medicineOncologymedicine.medical_specialtySkin NeoplasmsTime FactorsPhases of clinical researchYoung Adult03 medical and health scienceschemistry.chemical_compound0302 clinical medicineInternal medicineAntineoplastic Combined Chemotherapy ProtocolsBiomarkers TumormedicineHumansMolecular Targeted TherapyProgression-free survivalVemurafenibMelanomaProtein Kinase InhibitorsAgedAged 80 and overSulfonamidesPerformance statusbusiness.industryMelanomaMEK inhibitorBinimetinibMiddle Agedmedicine.diseaseProgression-Free Survival030104 developmental biologyVemurafenibOncologyTolerabilitychemistry030220 oncology & carcinogenesisMutationBenzimidazolesFemaleCarbamatesbusinessmedicine.drugThe Lancet Oncology
researchProduct

Erythema nodosum-like lesions during BRAF inhibitor therapy: Report on 16 new cases and review of the literature.

2015

Importance BRAF inhibitors have been licensed for the therapy of BRAF-mutated melanoma. Recently, inflammatory skin lesions clinically resembling erythema nodosum have been reported as therapy side-effects that may lead to treatment discontinuation. Objective To identify and characterize cases with BRAF inhibitor-associated erythema nodosum-like inflammatory skin lesions and development of an algorithm for their management. Design and Setting Retrospective chart review of melanoma patients treated with BRAF inhibitors in 14 departments of Dermatology in Germany and Austria and PubMed search for cases in the literature. Results Sixteen patients were identified who developed erythema nodosum-…

AdultMaleProto-Oncogene Proteins B-rafmedicine.medical_specialtyIndolesErythemaBiopsyMedizinDermatology030207 dermatology & venereal diseases03 medical and health sciencesYoung Adult0302 clinical medicineErythema NodosumOximesmedicineHumansskin and connective tissue diseasesVemurafenibneoplasmsAgedRetrospective StudiesSkinTrametinibErythema nodosumSulfonamidesintegumentary systembusiness.industryMelanomaImidazolesDabrafenibMiddle Agedmedicine.diseaseDermatology3. Good healthInfectious DiseasesVemurafenib030220 oncology & carcinogenesisFemalemedicine.symptombusinessPanniculitisVasculitismedicine.drugJournal of the European Academy of Dermatology and Venereology : JEADV
researchProduct

Adverse events associated with encorafenib plus binimetinib in the COLUMBUS study: incidence, course and management.

2019

Abstract Background Dual inhibition of the mitogen-activated protein kinase pathway with BRAF/MEK inhibitor (BRAFi/MEKi) therapy is a standard treatment for BRAFV600-mutant metastatic melanoma and has historically been associated with grade III pyrexia or photosensitivity depending on the combination used. The objective of this study was to fully describe adverse events from the COLUMBUS study evaluating the most recent BRAF/MEK inhibitor combination encorafenib+binimetinib. Patients and methods Patients with locally advanced, unresectable or metastatic BRAFV600-mutant melanoma were randomised to receive encorafenib 450 mg once daily plus binimetinib 45 mg twice daily, encorafenib 300 mg on…

Encorafenib0301 basic medicineOncologyMaleCancer ResearchSkin NeoplasmsBinimetinib; Encorafenib; Melanoma; Safety; Vemurafenib;MedizinBinimetinibchemistry.chemical_compound0302 clinical medicineAntineoplastic Combined Chemotherapy Protocols1306 Cancer ResearchVemurafenibMelanomaFatigueeducation.field_of_studySulfonamidesMEK inhibitorMelanomaStandard treatmentIncidence10177 Dermatology ClinicBinimetinibNauseaMiddle AgedOncology030220 oncology & carcinogenesis2730 OncologyFemaleSafetyMitogen-Activated Protein Kinasesmedicine.drugProto-Oncogene Proteins B-rafmedicine.medical_specialtyVomitingPopulation610 Medicine & health03 medical and health sciencesInternal medicinemedicineHumanseducationAdverse effectProtein Kinase Inhibitorsbusiness.industrymedicine.diseaseDiscontinuation030104 developmental biologychemistryVemurafenibMutationBenzimidazolesCarbamatesbusinessEuropean journal of cancer (Oxford, England : 1990)
researchProduct

Long-lasting tumor response on short-time administration of vemurafenib—A case report

2014

Vemurafenib has been approved since 2011 in the United States for the treatment of advanced BRAF V600–mutated melanoma as first-line therapy. Although it significantly prolongs overall and progression-free survival, most patients relapse within 6 to 8 months owing to acquisition of drug resistance. New findings suggest that discontinuous dose administration of vemurafenib might prolong response to vemurafenib, but it is unclear whether modified cell signalling or other mechanisms, such as immune-mediated effects, are responsible for this effect.

Long lastingOncologymedicine.medical_specialtybusiness.industryMelanomashort-time treatmentCase ReportDermatologyDrug resistancePharmacologyTumor responsemedicine.diseaseInternal medicinemelanomamedicinevemurafenibbusinessVemurafenibmedicine.drugJAAD Case Reports
researchProduct

The Genetic Landscape of Clinical Resistance to RAF Inhibition in Metastatic Melanoma.

2013

Abstract Most patients with BRAFV600-mutant metastatic melanoma develop resistance to selective RAF kinase inhibitors. The spectrum of clinical genetic resistance mechanisms to RAF inhibitors and options for salvage therapy are incompletely understood. We performed whole-exome sequencing on formalin-fixed, paraffin-embedded tumors from 45 patients with BRAFV600-mutant metastatic melanoma who received vemurafenib or dabrafenib monotherapy. Genetic alterations in known or putative RAF inhibitor resistance genes were observed in 23 of 45 patients (51%). Besides previously characterized alterations, we discovered a “long tail” of new mitogen-activated protein kinase (MAPK) pathway alterations (…

MAPK/ERK pathwayMelanomaMedizin10177 Dermatology ClinicSalvage therapy610 Medicine & healthDabrafenibDrug resistanceBiologymedicine.diseaseBioinformaticsMicrophthalmia-associated transcription factorArticleProto-Oncogene Proteins B-rafOncologyCancer researchmedicine2730 OncologyVemurafenibmedicine.drug
researchProduct

Abstract A292: Salinomycin, an anti-cancer stem cell antibiotic, overcomes acquired resistance to BRAF inhibitors in BRAF-mutant human melanoma cell …

2013

Abstract Advanced malignant melanoma is one of the most lethal cancers, because it is highly metastatic and refractory to conventional chemotherapy. About 60% of melanomas harbor oncogenic BRAF mutations which aberrantly activate MEK/ERK signaling pathway. BRAF and MEK inhibitors have been shown efficacious in patients with BRAF-mutant melanoma, but there is not effective target therapy for BRAF wild type melanomas. Unfortunately acquired resistance to BRAF targeted therapies is a common event: 50% of treated patients progressed within 6 to 7 months after the initiation of treatment. Resistance is associated with reactivation of the MAPK pathway (through development of de novo NRAS, NF1 or …

MAPK/ERK pathwayNeuroblastoma RAS viral oncogene homologCancer ResearchMelanomaWnt signaling pathwayCancerBiologymedicine.diseaseOncologyCancer stem cellImmunologymedicineCancer researchVemurafenibneoplasmsPI3K/AKT/mTOR pathwaymedicine.drugMolecular Cancer Therapeutics
researchProduct