Search results for "Proto-oncogene"

showing 10 items of 770 documents

Specific role of N-methyl-D-aspartate (NMDA) receptor in elastin-derived VGVAPG peptide-dependent calcium homeostasis in mouse cortical astrocytes in…

2019

AbstractUnder physiological and pathological conditions, elastin is degraded to produce elastin-derived peptides (EDPs). EDPs are detected in the healthy human brain, and its concentration significantly increases after ischemic stroke. Both elastin and EDPs contains replications of the soluble VGVAPG hexapeptide, which has a broad range of biological activities. Effects of VGVAPG action are mainly mediated by elastin-binding protein (EBP), which is alternatively spliced, enzymatically inactive form of the GLB1 gene. This study was conducted to elucidate the activation and role of the N-methyl-D-aspartate receptor (NMDAR) in elastin-derived VGVAPG peptide-dependent calcium homeostasis in mou…

0301 basic medicineMolecular biologylcsh:MedicinePathogenesisBiochemistryReceptors N-Methyl-D-AspartateArticleMice03 medical and health sciencesMedical research0302 clinical medicineAnimalsHomeostasisGene silencingGene SilencingRNA MessengerRNA Small InterferingReceptorlcsh:ScienceCells CulturedCerebral CortexGene knockdownMultidisciplinaryMolecular medicinebiologyChemistrylcsh:RIn vitroElastinCell biology030104 developmental biologyAstrocytesbiology.proteinNMDA receptorCalciumlcsh:QSignal transductionReactive Oxygen SpeciesOligopeptidesElastinBiomarkers030217 neurology & neurosurgeryProto-oncogene tyrosine-protein kinase SrcScientific Reports
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Impact of BRAF and RAS mutations on first-line efficacy of FOLFIRI plus cetuximab versus FOLFIRI plus bevacizumab: analysis of the FIRE-3 (AIO KRK-03…

2017

Abstract Background RAS and BRAF mutations have been identified as negative prognostic factors in metastatic colorectal cancer. Efficacy of 5-fluorouracil, leucovorin, irinotecan (FOLFIRI) plus bevacizumab in patients with RAS-mutant tumours needs to be further evaluated. Whether to treat patients with BRAF-mutant tumours with either bevacizumab or anti-epidermal growth factor receptor (EGFR) antibodies remains unclear. Methods Patients treated within the FIRE-3 trial were retrospectively tested for BRAF and RAS mutations using formalin fixated paraffin embedded (FFPE) tumour material applying pyrosequencing for KRAS and NRAS exon 2, 3 and 4 mutations as far as for BRAF mutations. Survival …

0301 basic medicineNeuroblastoma RAS viral oncogene homologOncologyMaleProto-Oncogene Proteins B-rafCancer Researchmedicine.medical_specialtyBevacizumabColorectal cancerLeucovorinCetuximabmedicine.disease_causeProto-Oncogene Proteins p21(ras)03 medical and health sciences0302 clinical medicineInternal medicineAntineoplastic Combined Chemotherapy ProtocolsmedicineHumansneoplasmsSurvival analysisAgedRetrospective StudiesCetuximabbusiness.industryLiver NeoplasmsExonsMiddle Agedmedicine.diseasedigestive system diseasesIrinotecanBevacizumab030104 developmental biologyTreatment OutcomeOncology030220 oncology & carcinogenesisMutationFOLFIRICamptothecinFemaleKRASFluorouracilbusinessColorectal Neoplasmsmedicine.drugEuropean journal of cancer (Oxford, England : 1990)
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Does bevacizumab impact anti-EGFR therapy efficacy in metastatic colorectal cancer?

2016

IF 5.008; International audience; Anti-EGFR therapy and antiangiogenic therapies are used alone or in combination with chemotherapies to improve survival in metastatic colorectal cancer. However, it is unknown whether pretreatment with antiangiogenic therapy could impact on the efficacy of anti-EGFR therapy. We selected one hundred and twenty eight patients diagnosed with advanced colorectal cancer with a KRAS and NRAS unmutated tumor. These patients were treated with cetuximab or panitumumab alone or with chemotherapy as second or third-line. Univariate and multivariate Cox model analysis were performed to estimate the effect of a previous bevacizumab regimen on progression free survival a…

0301 basic medicineNeuroblastoma RAS viral oncogene homologOncologyMaleVascular Endothelial Growth Factor AColorectal cancerCetuximabAngiogenesis Inhibitorsmedicine.disease_causeTrialGTP PhosphohydrolasesRas mutations[ SDV.CAN ] Life Sciences [q-bio]/Cancer0302 clinical medicineAntineoplastic Combined Chemotherapy ProtocolsDrug InteractionsAged 80 and overCetuximabPanitumumabAntibodies MonoclonalMiddle Aged3. Good healthErbB ReceptorsOncology030220 oncology & carcinogenesisFemaleKRASColorectal Neoplasms1st-Line treatmentmedicine.drugResearch PaperAdultSTAT3 Transcription Factormedicine.medical_specialtyBevacizumabAntineoplastic Agents[SDV.CAN]Life Sciences [q-bio]/Cancer[SDV.BC]Life Sciences [q-bio]/Cellular BiologybevacizumabIrinotecanDisease-Free SurvivalTumor angiogenesisProto-Oncogene Proteins p21(ras)03 medical and health sciencesVEGFRInternal medicineCell Line TumormedicinePanitumumabHumansEndothelial growth-FactorChemotherapyProgression-free survivalAgedbusiness.industry[ SDV.BC ] Life Sciences [q-bio]/Cellular BiologyMembrane Proteinsmetastatic colon cancerStat-3medicine.diseaseVascular Endothelial Growth Factor Receptor-2IrinotecanRandomized phase-III030104 developmental biologyanti-EGFR therapyFactor receptorCaco-2 Cellsbusiness
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Genomic Amplifications and Distal 6q Loss: Novel Markers for Poor Survival in High-risk Neuroblastoma Patients.

2018

Abstract Background Neuroblastoma is characterized by substantial clinical heterogeneity. Despite intensive treatment, the survival rates of high-risk neuroblastoma patients are still disappointingly low. Somatic chromosomal copy number aberrations have been shown to be associated with patient outcome, particularly in low- and intermediate-risk neuroblastoma patients. To improve outcome prediction in high-risk neuroblastoma, we aimed to design a prognostic classification method based on copy number aberrations. Methods In an international collaboration, normalized high-resolution DNA copy number data (arrayCGH and SNP arrays) from 556 high-risk neuroblastomas obtained at diagnosis were coll…

0301 basic medicineOncologyCancer ResearchSomatic cellNeuroblastoma0302 clinical medicineGene duplicationMedicine and Health SciencesHigh risk neuroblastomaN-Myc Proto-Oncogene ProteinABNORMALITIESIntensive treatmentGenomicsArticlesPrognosis3. Good healthOncologyChild Preschool030220 oncology & carcinogenesisChromosomes Human Pair 6Chromosome DeletionINTEGRATIONmedicine.medical_specialtyDNA Copy Number VariationsCLASSIFICATION03 medical and health sciencesAGEInternal medicineNeuroblastomaSTRATIFICATIONClinical heterogeneityBiomarkers TumormedicineHumansGenetic Predisposition to DiseaseCopy number aberrationneoplasmsGenetic Association StudiesNeoplasm StagingACCUMULATIONbusiness.industryOUTCOME PREDICTIONGene AmplificationInfantBiology and Life SciencesDNAmedicine.diseaseDELINEATION030104 developmental biologyCOPY NUMBEROutcome predictionbusiness
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Focal Adhesion Genes Refine the Intermediate-Risk Cytogenetic Classification of Acute Myeloid Leukemia

2018

© 2018 by the authors.

0301 basic medicineOncologyCancer Researchmedicine.medical_specialtyNPM1PTK2acute myeloid leukemialcsh:RC254-282Article03 medical and health sciences0302 clinical medicinePTK2BLYNInternal medicinehemic and lymphatic diseasesmedicineLYNprognostic factorPrognostic factorintermediate-riskPTK2BAcute myeloid leukemiaPTK2business.industryMyeloid leukemialcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens030104 developmental biologyOncology030220 oncology & carcinogenesisCohortIntermediate-riskbusinessTyrosine kinaseProto-oncogene tyrosine-protein kinase SrcCancers
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Detection of MET Alterations Using Cell Free DNA and Circulating Tumor Cells from Cancer Patients

2020

MET alterations may provide a potential biomarker to evaluate patients who will benefit from treatment with MET inhibitors. Therefore, the purpose of the present study is to investigate the utility of a liquid biopsy-based strategy to assess MET alterations in cancer patients. We analyzed MET amplification in circulating free DNA (cfDNA) from 174 patients with cancer and 49 healthy controls and demonstrated the accuracy of the analysis to detect its alteration in patients. Importantly, a significant correlation between cfDNA concentration and MET copy number (CN) in cancer patients (r = 0.57, p &lt

0301 basic medicineOncologyMale<i>MET</i> copy numbermedicine.medical_treatmentproteínas protooncogénicas c-metdosificación génicahumanosresistencia a medicamentosDrug ResistanceGene Dosagecirculating free DNA (cfDNA)<i>MET</i> amplificationTargeted therapyTargeted therapy0302 clinical medicineCirculating tumor cellestudios prospectivosNeoplasmsantineoplásicosProspective Studieslcsh:QH301-705.5Circulating tumor cells (CTCs)neoplasiasGeneral MedicineProto-Oncogene Proteins c-mettargeted therapyNeoplastic Cells CirculatingErbB ReceptorsCell-free fetal DNA030220 oncology & carcinogenesisinhibidores de proteína cinasasBiomarker (medicine)FemaleMET protein expressionCell-Free Nucleic AcidsMET amplificationmedicine.medical_specialtycirculating tumor cells (CTCs)estudios de casos y controlesMet amplificationCirculating free DNA (cfDNA)Antineoplastic AgentsArticle03 medical and health sciencesInternal medicinemedicineBiomarkers TumorHumansLiquid biopsyProtein Kinase InhibitorsRetrospective Studiesbusiness.industryHead and neck cancerestudios retrospectivosLiquid BiopsyCancermedicine.disease030104 developmental biologylcsh:Biology (General)Drug Resistance NeoplasmCase-Control StudiesMET copy numberbusinessCells
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Phospho-Akt overexpression is prognostic and can be used to tailor the synergistic interaction of Akt inhibitors with gemcitabine in pancreatic cancer

2017

Background There is increasing evidence of a constitutive activation of Akt in pancreatic ductal adenocarcinoma (PDAC), associated with poor prognosis and chemoresistance. Therefore, we evaluated the expression of phospho-Akt in PDAC tissues and cells, and investigated molecular mechanisms influencing the therapeutic potential of Akt inhibition in combination with gemcitabine. Methods Phospho-Akt expression was evaluated by immunohistochemistry in tissue microarrays (TMAs) with specimens tissue from radically-resected patients (n = 100). Data were analyzed by Fisher and log-rank test. In vitro studies were performed in 14 PDAC cells, including seven primary cultures, characterized for their…

0301 basic medicineOncologyMaleCancer ResearchBiopsyAKT1ApoptosisAkt; Gemcitabine; Pancreatic ductal adenocarcinoma; Synergism; Hematology; Molecular Biology; Oncology; Cancer ResearchDeoxycytidinePancreatic ductal adenocarcinoma0302 clinical medicineCell MovementTumor Cells CulturedGlucose Transporter Type 1medicine.diagnostic_testChemistryCell CyclePancreatic NeoplasmDrug Synergismlcsh:Diseases of the blood and blood-forming organsHematologyCell cycleMiddle Agedlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPrognosisOncologyAkt; Gemcitabine; Pancreatic ductal adenocarcinoma; Synergism; Aged; Apoptosis; Biopsy; Carcinoma Pancreatic Ductal; Cell Cycle; Cell Movement; Deoxycytidine; Drug Synergism; Female; Glucose Transporter Type 1; Humans; Male; Middle Aged; Pancreatic Neoplasms; Phosphoproteins; Prognosis; Proto-Oncogene Proteins c-akt; RNA Messenger; Spheroids Cellular; Tumor Cells Cultured; Hematology; Molecular Biology; Oncology; Cancer Research030220 oncology & carcinogenesisPhosphoproteinFemalemedicine.drugHumanCarcinoma Pancreatic Ductalmedicine.medical_specialtyPrognosilcsh:RC254-282Flow cytometry03 medical and health sciencesInternal medicinePancreatic cancerSpheroids CellularmedicineHumansRNA MessengerProtein kinase BMolecular BiologyPI3K/AKT/mTOR pathwayAgedlcsh:RC633-647.5ResearchAktSynergismApoptosimedicine.diseasePhosphoproteinsGemcitabineGemcitabinePancreatic Neoplasms030104 developmental biologyCancer cellCancer researchProto-Oncogene Proteins c-akt
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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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