Search results for "Oncogene protein"

showing 10 items of 812 documents

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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miR‐200c and phospho‐AKT as prognostic factors and mediators of osteosarcoma progression and lung metastasis

2016

Lung metastasis is the major cause of death in osteosarcoma patients. However, molecular mechanisms underlying this metastasis remain poorly understood. To identify key molecules related with pulmonary metastasis of pediatric osteosarcomas, we analyzed high-throughput miRNA expression in a cohort of 11 primary tumors and 15 lung metastases. Results were further validated with an independent cohort of 10 primary tumors and 6 metastases. In parallel, we performed immunohistochemical analysis of activated signaling pathways in 36 primary osteosarcomas. Only phospho-AKT associated with lower overall survival in primary tumors, supporting its role in osteosarcoma progression. CTNNB1 expression a…

0301 basic medicineOncologyMaleCancer ResearchmiR‐200cLung NeoplasmsCDH1MetastasisCohort Studies0302 clinical medicineCell MovementPhospho‐AKTPhosphorylationChildOsteosarcomabiologyGeneral MedicineArticlesCadherinsPrognosisPrimary tumorGene Expression Regulation Neoplasticmedicine.anatomical_structureLung metastasisOncology030220 oncology & carcinogenesisDisease ProgressionMolecular MedicineOsteosarcomaFemaleSignal Transductionmedicine.medical_specialtyAdolescentMesenchymal to epithelial transitionArticle03 medical and health sciencesYoung AdultAntigens CDInternal medicineCell Line TumormicroRNAGeneticsmedicineBiomarkers TumorHumansEpithelial–mesenchymal transitionCell ProliferationLungGene Expression ProfilingReproducibility of ResultsEpithelial CellsPediatric osteosarcomamedicine.diseaseSurvival AnalysisEnzyme ActivationMicroRNAs030104 developmental biologyTumor progressionbiology.proteinProto-Oncogene Proteins c-aktMolecular Oncology
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Prevalence and clinical association of gene mutations through multiplex mutation testing in patients with NSCLC

2017

[EN] Background Reported prevalence of driver gene mutations in non-small-cell lung cancer (NSCLC) is highly variable and clinical correlations are emerging. Using NSCLC biomaterial and clinical data from the European Thoracic Oncology Platform Lungscape iBiobank, we explore the epidemiology of mutations and association to clinicopathologic features and patient outcome (relapse-free survival, time-to-relapse, overall survival). Methods Clinically annotated, resected stage I¿III NSCLC FFPE tissue was assessed for gene mutation using a microfluidics-based multiplex PCR platform. Mutant-allele detection sensitivity is¿>1% for most of the ~150 (13 genes) mutations covered in the multiplex test.…

0301 basic medicineOncologyMaleLung NeoplasmsDNA Mutational AnalysisKRAS MUTATIONSGene mutationmedicine.disease_cause0302 clinical medicinemultiplex mutation analysisCarcinoma Non-Small-Cell LungMultiplex mutation analysisPrevalenceMultiplexAnaplastic Lymphoma KinaseHETEROGENEITYAged 80 and overMutationSmokingHematologyMiddle AgedProto-Oncogene Proteins c-metProgression-Free SurvivalOncology030220 oncology & carcinogenesisAdenocarcinomaFemaleKRASPREDICT SURVIVALAdultmedicine.medical_specialtyEGFRCELL LUNG-CANCERPrognosis molecular stagingprognosis molecular stagingEGFR KRAS PIK3CAVALIDATION03 medical and health sciencesYoung AdultInternal medicineMultiplex polymerase chain reactionmedicineKRASTYROSINE KINASE INHIBITORSHumansProgression-free survivalLung cancerAgedNeoplasm Stagingbusiness.industryMICROBIOLOGIAADENOCARCINOMAAMPLIFICATIONPIK3CAmedicine.disease030104 developmental biologynon-small-cell lung cancerMutationOVEREXPRESSIONbusinessMultiplex Polymerase Chain ReactionNon-small-cell lung cancerAnnals of Oncology
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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
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Can KRAS and BRAF mutations limit the benefit of liver resection in metastatic colorectal cancer patients? A systematic review and meta-analysis.

2016

Clinical trials investigated the potential role of both KRAS and BRAF mutations, as prognostic biomarkers, in colorectal cancer (CRC) patients who underwent surgical treatment of CRC-related liver metastases (CLM), showing conflicting results. This meta-analysis aims to review all the studies reporting survival outcomes (recurrence free survival (RFS), and/or overall survival (OS)) of patients undergoing resection of CLM, stratified according to KRAS and/or BRAF mutation status. Background: Clinical trials investigated the potential role of both KRAS and BRAF mutations, as prognostic biomarkers, in colorectal cancer (CRC) patients who underwent surgical treatment of CRC-related liver metast…

0301 basic medicineOncologyendocrine system diseasesColorectal cancerLiver metastasimedicine.medical_treatmentColorectal Neoplasmmedicine.disease_cause0302 clinical medicineLiver metastasisHematologyTumorLiver NeoplasmsHematologyPrognosisSurvival RateOncologyLiver Neoplasm030220 oncology & carcinogenesisMeta-analysisKRASColorectal NeoplasmsHumanProto-Oncogene Proteins B-rafmedicine.medical_specialtyPrognostic biomarkerPrognosiResectionBRAFProto-Oncogene Proteins p21(ras)03 medical and health sciencesInternal medicineBRAF; Colorectal cancer; KRAS; Liver metastasis; Prognostic biomarker; Biomarkers Tumor; Colorectal Neoplasms; Humans; Liver Neoplasms; Mutation; Prognosis; Proto-Oncogene Proteins B-raf; Proto-Oncogene Proteins p21(ras); Survival Rate; Hepatectomy; Oncology; Hematology; Geriatrics and GerontologymedicineKRASBiomarkers TumorHepatectomyHumansneoplasmsSurvival ratebusiness.industrymedicine.diseaseColorectal cancerdigestive system diseasesClinical trial030104 developmental biologyMutationBRAF; Colorectal cancer; KRAS; Liver metastasis; Prognostic biomarker; Biomarkers; Tumor; Colorectal Neoplasms; Humans; Liver Neoplasms; Mutation; Prognosis; Proto-Oncogene Proteins B-raf; Proto-Oncogene Proteins p21(ras); Survival Rate; Hepatectomy; Oncology; Hematology; Geriatrics and GerontologyHepatectomyGeriatrics and GerontologybusinessBiomarkersCritical reviews in oncology/hematology
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Immunohistochemical analysis of NKX2.2, ETV4, and BCOR in a large series of genetically confirmed Ewing sarcoma family of tumors

2017

Ewing sarcoma is an aggressive neoplasm of pediatric and adolescent patients. Immunohistochemistry (IHC) can be used to support the morphologic diagnosis of Ewing sarcoma family of tumors (ESFT) in a convincing clinical/radiological context. Although neither NKX2.2 nor CD99 alone are entirely specific, when combined, the diagnostic specificity is high. The aim of the present study was to investigate the IHC expression of NKX2.2, ETV4 and BCOR in a large series of genetically confirmed ESFT. The results for CD99 and CAV-1 immunoreactivity, and the histological and fusion gene subtypes were retrieved from our previous study. NKX2.2 demonstrated moderate or strong nuclear positivity in 91.2% o…

0301 basic medicinePathologymedicine.medical_specialtyCD99Bone NeoplasmsContext (language use)Sarcoma EwingBiologyPathology and Forensic MedicineFusion gene03 medical and health sciences0302 clinical medicineProto-Oncogene ProteinsBiomarkers TumormedicineHumansNeoplasmHomeodomain ProteinsProto-Oncogene Proteins c-etsNuclear ProteinsCell BiologyZebrafish Proteinsmedicine.diseaseImmunohistochemistryRepressor ProteinsHomeobox Protein Nkx-2.2030104 developmental biology030220 oncology & carcinogenesisCancer researchbiology.proteinImmunohistochemistryAdenovirus E1A ProteinsSarcomaMorphologic diagnosisAntibodyTranscription FactorsPathology - Research and Practice
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