Search results for "In [ZnO]"

showing 10 items of 1883 documents

Compassionate use of everolimus for refractory epilepsy in a patient with MTOR mosaic mutation

2020

Abstract The MTOR gene encodes the mechanistic target of rapamycin (mTOR), which is a core component of the PI3K-AKT-mTOR signaling pathway. Postzygotic MTOR variants result in various mosaic phenotypes, referred to in OMIM as Smith-Kinsgmore syndrome or focal cortical dysplasia. We report here the case of a patient, with an MTOR mosaic gain-of-function variant (p.Glu2419Lys) in the DNA of 41% skin cells, who received compassionate off-label treatment with everolimus for refractory epilepsy. This 12-year-old-girl presented with psychomotor regression, intractable seizures, hypopigmentation along Blaschko's lines (hypomelanosis of Ito), asymmetric regional body overgrowth, and ocular anomali…

0301 basic medicineOncologyCompassionate Use Trialsmedicine.medical_specialty[SDV]Life Sciences [q-bio]030105 genetics & heredityMuscle hypertrophyCraniofacial Abnormalities03 medical and health sciencesInternal medicineGeneticsmedicineHumansEverolimusChildMechanistic target of rapamycinProtein Kinase InhibitorsGenetics (clinical)PI3K/AKT/mTOR pathwayHypopigmentationEverolimusbiologybusiness.industryMosaicismTOR Serine-Threonine KinasesNeuropsychologyGeneral MedicineCortical dysplasiamedicine.disease3. Good healthClinical trialMalformations of Cortical Development[SDV] Life Sciences [q-bio]030104 developmental biologyPhenotypeGain of Function Mutationbiology.proteinFemaleEpilepsies Partialmedicine.symptombusinessmedicine.drug
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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
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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
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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)
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Immune checkpoint inhibition therapy for advanced skin cancer in patients with concomitant hematological malignancy: a retrospective multicenter DeCO…

2020

BackgroundSkin cancers are known for their strong immunogenicity, which may contribute to a high treatment efficacy of immune checkpoint inhibition (ICI). However, a considerable proportion of patients with skin cancer is immuno-compromised by concomitant diseases. Due to their previous exclusion from clinical trials, the ICI treatment efficacy is poorly investigated in these patients. The present study analyzed the ICI treatment outcome in advanced patients with skin cancer with a concomitant hematological malignancy.MethodsThis retrospective multicenter study included patients who were treated with ICI for locally advanced or metastatic melanoma (MM), cutaneous squamous cell carcinoma (cS…

0301 basic medicineOncologyMaleCancer Researchmedicine.medical_specialtySkin Neoplasms2435medicine.medical_treatmentChronic lymphocytic leukemiaImmunologyMedizin03 medical and health sciences0302 clinical medicineInternal medicinemedicinemelanomaImmunology and AllergyHumans1506Immune Checkpoint InhibitorsRC254-282AgedRetrospective StudiesPharmacologyClinical/Translational Cancer ImmunotherapyMerkel cell carcinomabusiness.industryMelanomaNeoplasms. Tumors. Oncology. Including cancer and carcinogensImmunotherapyMiddle Agedmedicine.diseaseSurvival AnalysisLymphoma030104 developmental biologyOncology030220 oncology & carcinogenesisConcomitantHematologic NeoplasmsMolecular MedicineFemaleImmunotherapySkin cancerbusinessProgressive diseaseJournal for Immunotherapy of Cancer
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Associations of Pathogenic Variants in MLH1, MSH2, and MSH6 With Risk of Colorectal Adenomas and Tumors and With Somatic Mutations in Patients With L…

2020

Contains fulltext : 220040.pdf (Publisher’s version ) (Closed access) BACKGROUND & AIMS: Lynch syndrome is caused by variants in DNA mismatch repair (MMR) genes and associated with an increased risk of colorectal cancer (CRC). In patients with Lynch syndrome, CRCs can develop via different pathways. We studied associations between Lynch syndrome-associated variants in MMR genes and risks of adenoma and CRC and somatic mutations in APC and CTNNB1 in tumors in an international cohort of patients. METHODS: We combined clinical and molecular data from 3 studies. We obtained clinical data from 2747 patients with Lynch syndrome associated with variants in MLH1, MSH2, or MSH6 from Germany, the Net…

0301 basic medicineOncologyMaleColorectal cancerDNA Mutational Analysisgenetic analysisHEREDITARYcancer riskGUIDELINESDNA Mismatch Repair0302 clinical medicineGermanyTumours of the digestive tract Radboud Institute for Molecular Life Sciences [Radboudumc 14]Prospective Studiesprognostic factorFinlandbeta CateninNetherlandsOutcomePrognostic FactorGastroenterologyGenetic AnalysisColonoscopyMiddle AgedCANCERLynch syndromeCancer Risk3. Good healthDNA-Binding ProteinsDEFICIENCYMutS Homolog 2 Proteinsyöpägeenitoutcome030211 gastroenterology & hepatologyDNA mismatch repairFemaleMutL Protein Homolog 1geenitutkimusAdenomaAdultmedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesAdenoma3122 CancersAdenomatous Polyposis Coli ProteinINSTABILITYSOCIETYMLH103 medical and health sciencesInternal medicinemedicineMANAGEMENTHumansLynchin oireyhtymäneoplasmspaksusuolisyöpäHepatologybusiness.industryCancernutritional and metabolic diseasesennusteetmedicine.diseaseColorectal Neoplasms Hereditary Nonpolyposisdigestive system diseasesMSH6030104 developmental biologyMSH2Mutationbusiness
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Blood baseline neutrophil count predicts bevacizumab efficacy in glioblastoma

2016

// Aurelie Bertaut 1 , Caroline Truntzer 2 , Rachid Madkouri 3 , Coureche Guillaume Kaderbhai 4 , Valentin Derangere 5 , Julie Vincent 4 , Bruno Chauffert 6 , Marie Helene Aubriot-Lorton 7 , Wahlid Farah 3 , Klaus Luc Mourier 3 , Romain Boidot 5,8 and Francois Ghiringhelli 4,5,8,9 1 Biostatistics unit Georges Francois Leclerc Cancer Center, Dijon, France 2 CLIPP, Research Center, University of Burgundy, Dijon, France 3 Department of Neurosurgery, CHU, Dijon, France 4 Department of Medical Oncology, Georges Francois Leclerc Cancer Center, Dijon, France 5 Platform of Transfer in Cancer Biology Genetic and histology, Georges Francois Leclerc Cancer Center, Dijon, France 6 Department of Medical…

0301 basic medicineOncologyMaleVascular Endothelial Growth Factor Agenetic structuresNeutrophilsmedicine.medical_treatmentAngiogenesis InhibitorsBiomarkers Pharmacological[ SDV.CAN ] Life Sciences [q-bio]/CancerLeukocyte Count0302 clinical medicineAntineoplastic Combined Chemotherapy ProtocolsGranulocyte Colony-Stimulating FactorEndothelial Growth-Factorprognostic factorNeoadjuvant therapyRandomized Controlled Trials as TopicNeovascularization PathologicBrain NeoplasmsColony-Stimulating FactorAge FactorsChemoradiotherapyMiddle AgedPrognosisNeoadjuvant Therapy3. Good healthTreatment OutcomeOncology030220 oncology & carcinogenesisTo-Lymphocyte RatioAbsolute neutrophil countFemalemedicine.drugmedicine.medical_specialtyBevacizumabMalignant Glioma[SDV.CAN]Life Sciences [q-bio]/Cancer[SDV.BC]Life Sciences [q-bio]/Cellular BiologybevacizumabDisease-Free Survival03 medical and health sciencesInternal medicinemedicineHumansPretreatment NeutrophilKarnofsky Performance StatusSingle-Agent BevacizumabRetrospective StudiesNewly-Diagnosed GlioblastomaRecurrent Glioblastomabusiness.industry[ SDV.BC ] Life Sciences [q-bio]/Cellular BiologyGene Expression ProfilingglioblastomaCancerRetrospective cohort studyLomustinemedicine.diseasePhase-Ii Trialeye diseasesSurgeryIrinotecan030104 developmental biologyprognosistic factorBrain-Tumorssense organsClinical Research PaperNeoplasm Recurrence LocalbusinessChemoradiotherapyFollow-Up Studies
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Oxidative signature of cerebrospinal fluid from mild cognitive impairment and Alzheimer disease patients

2015

Abstract Background Several studies suggest that pathological changes in Alzheimer’s disease (AD) brain begin around 10–20 years before the onset of cognitive impairment. Biomarkers that can support early diagnosis and predict development of dementia would, therefore, be crucial for patient care and evaluation of drug efficacy. Although cerebrospinal fluid (CSF) levels of Aβ42, tau, and p-tau are well-established diagnostic biomarkers of AD, there is an urgent need to identify additional molecular alterations of neuronal function that can be evaluated at the systemic level. Objectives This study was focused on the analysis of oxidative stress-related modifications of the CSF proteome, from …

0301 basic medicineOncologyPathologyDiseasephysiology (medical)medicine.disease_causeProtein oxidationtau proteins0302 clinical medicineCerebrospinal fluidmiddle aged80 and overoxidative stresshumansAged 80 and overamyloid beta-peptidesredox proteomicsagedfemale030220 oncology & carcinogenesisBiomarker (medicine)Alzheimer's diseaseAlzheimer diseaseAPOEmedicine.medical_specialtyoxidation-reductionproteomeCSFmolecular sequence data03 medical and health sciencesmalecognitive dysfunctionInternal medicinemental disordersmedicineDementiabiochemistryprotein oxidationbusiness.industrypeptide fragmentscase-control studiesCase-control studybiomarkersmedicine.diseaseAPOE; biomarkers; CSF; extracellular chaperones; protein oxidation; redox proteomics; aged; aged 80 and over; Alzheimer disease; amino acid sequence; amyloid beta-peptides; apolipoproteins E; biomarkers; case-control studies; cognitive dysfunction; female; humans; male; middle aged; molecular sequence data; oxidation-reduction; oxidative stress; peptide fragments; proteome; tau proteins; biochemistry; physiology (medical)extracellular chaperonesamino acid sequence030104 developmental biologybusinessOxidative stressapolipoproteins E
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Does breast carcinoma belong to the Lynch syndrome tumor spectrum? : Somatic mutational profiles vs. ovarian and colorectal carcinomas

2020

// Noora K. Porkka 1 , Alisa Olkinuora 1 , Teijo Kuopio 2 , 3 , Maarit Ahtiainen 4 , Samuli Eldfors 5 , Henrikki Almusa 5 , Jukka-Pekka Mecklin 6 , 7 , 8 and Paivi Peltomaki 1 1 Department of Medical and Clinical Genetics, University of Helsinki, Helsinki, Finland 2 Department of Pathology, Jyvaskyla Central Hospital, Jyvaskyla, Finland 3 Department of Biological and Environmental Science, University of Jyvaskyla, Jyvaskyla, Finland 4 Department of Education and Research, Jyvaskyla Central Hospital and University of Eastern Finland, Jyvaskyla, Finland 5 Institute for Molecular Medicine Finland, University of Helsinki, Helsinki, Finland 6 Faculty of Sport and Health Sciences, University of J…

0301 basic medicineOncologymedicine.medical_specialtyDNA mismatch repair3122 Cancersmedicine.disease_cause03 medical and health sciences0302 clinical medicineBreast cancerGermline mutationInternal medicinemedicinesomatic mutationbreast carcinomaLynchin oireyhtymäMSIperinnölliset tauditrintasyöpäbusiness.industryCancermedicine.diseaseLynch syndromedigestive system diseases3. Good health030104 developmental biologyLynch syndromeOncologysyöpägeenit030220 oncology & carcinogenesisMedical geneticsDNA mismatch repairsyöpätaudit3111 BiomedicinemutaatiotCarcinogenesisBreast carcinomabusinessResearch Paper
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Current treatment options for HER2-positive breast cancer patients with brain metastases

2020

Abstract Brain metastases (BMs) are frequently associated with HER2+ breast cancer (BC). Their management is based on a multi-modal strategy including both local treatment and systemic therapy. Despite therapeutic advance, BMs still have an adverse impact on survival and quality of life and the development of effective systemic therapy to prevent and treat BMs from HER2 + BC represents an unmet clinical need. Trastuzumab-based therapy has long been the mainstay of systemic therapy and over the last two decades other HER2-targeted agents including lapatinib, pertuzumab and trastuzumab emtansine, have been introduced in the clinical practice. More recently, novel agents such as neratinib, tuc…

0301 basic medicineOncologymedicine.medical_specialtyPyridinesReceptor ErbB-2NeratinibTrastuzumab-emtansineBreast NeoplasmsLapatinibSystemic therapy03 medical and health scienceschemistry.chemical_compound0302 clinical medicineBreast cancerQuality of lifeTrastuzumabInternal medicineAntineoplastic Combined Chemotherapy ProtocolsmedicineHumansTrastuzumab deruxtecanHER2-positive breast cancerskin and connective tissue diseasesOxazolesneoplasmsTucatinibBrain Neoplasmsbusiness.industryBrain metastasesLapatinibHematologyTrastuzumabmedicine.disease030104 developmental biologyOncologychemistryTrastuzumab emtansine030220 oncology & carcinogenesisNeratinibQuality of LifeQuinazolinesPertuzumabbusinessmedicine.drugCritical Reviews in Oncology/Hematology
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