Search results for "TYROSINE KINASE"

showing 10 items of 362 documents

Intermittent targeted therapies and stochastic evolution in patients affected by chronic myeloid leukemia

2016

Front line therapy for the treatment of patients affected by chronic myeloid leukemia (CML) is based on the administration of tyrosine kinase inhibitors, namely imatinib or, more recently, axitinib. Although imatinib is highly effective and represents an example of a successful molecular targeted therapy, the appearance of resistance is observed in a proportion of patients, especially those in advanced stages. In this work, we investigate the appearance of resistance in patients affected by CML, by modeling the evolutionary dynamics of cancerous cell populations in a simulated patient treated by an intermittent targeted therapy. We simulate, with the Monte Carlo method, the stochastic evolu…

0301 basic medicineOncologyDrugStatistics and Probabilitymedicine.medical_specialtymedicine.medical_treatmentmedia_common.quotation_subjectTargeted therapy03 medical and health sciencesClassical Monte Carlo simulations; computational biology; models for evolution (theory); mutational and evolutionary processes (theory); Statistical and Nonlinear Physics; Statistics and Probability; Statistics Probability and Uncertainty0302 clinical medicinecomputational biologyInternal medicinemedicineClassical Monte Carlo simulationmutational and evolutionary processes (theory)media_commonbusiness.industryMyeloid leukemiaStatistical and Nonlinear PhysicsImatinibSettore FIS/07 - Fisica Applicata(Beni Culturali Ambientali Biol.e Medicin)Axitinib030104 developmental biology030220 oncology & carcinogenesisCancer cellToxicityStatistics Probability and Uncertaintybusinessmodels for evolution (theory)Tyrosine kinasemedicine.drugStatistical and Nonlinear Physic
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Comprehensive cross-platform comparison of methods for non-invasive EGFR mutation testing : results of the RING observational trial

2020

Plasma samples from 72 EGFR‐mutant advanced NSCLC patients, collected upon progression to first‐line TKI, were analyzed by seven methodologies (two NGS‐based methods, three high‐sensitivity PCR‐based platforms, and two FDA‐approved methods). Our study demonstrates a good to excellent agreement between methodologies and supports the use of liquid biopsies for therapy decision‐making.

0301 basic medicineOncologyMaleCancer Researchcell lung cancerIntraclass correlationBiopsyDNA Mutational Analysisnon-small cell lung cancer (NSCLC)Tyrosine kinase inhibitorTyrosine-kinase inhibitorCohort Studies*circulating free DNAT790M0302 clinical medicinetyrosine kinase inhibitorGene FrequencyOsimertinibProspective cohort studyCàncernon‐small‐cell lung cancerCirculating free DNARC254-282Research ArticlesSequence DeletionAged 80 and overNeoplasms. Tumors. Oncology. Including cancer and carcinogensHigh-Throughput Nucleotide Sequencingnon&#8208General MedicineDNA NeoplasmExonsMiddle AgedErbB ReceptorsEpidermal growth factor receptor (EGFR) NGS Non-small cell lung cancer (NSCLC) PCR Tyrosine Kinase Inhibitor (TKI) circulating free DNA (cfDNA) osimertinibOncology030220 oncology & carcinogenesisosimertinibNGSMolecular Medicinesmall&#8208FemaleResearch Article*NGSAdultmedicine.medical_specialtymedicine.drug_classSensitivity and Specificity03 medical and health sciencesPredictive Value of TestsInternal medicineGeneticsmedicineHumansAged*non-small-cell lung cancerbusiness.industryEpidermal growth factor receptorNon invasive*epidermal growth factor receptormedicine.disease*tyrosine kinase inhibitorrespiratory tract diseases030104 developmental biologyEgfr mutationPulmonsMutationcirculating free DNAbusinessepidermal growth factor receptorNon-small-cell lung cancer*osimertinibOsimertinib
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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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Cardiovascular Issues in Tyrosine Kinase Inhibitors Treatments for Chronic Myeloid Leukemia: A Review

2021

Chronic myeloid leukemia (CML) is a myeloproliferative neoplasm driven by a fusion gene, encoding for the chimeric protein BCR-ABL, with constitutive tyrosine kinase activity. The use of tyrosine kinase inhibitors (TKIs) has drastically improved survival, but there are significant concerns about cardiovascular toxicity. Cardiovascular risk can be lowered with appropriate baseline evaluation, accurate choice of TKI therapy, improvement of modifiable cardiovascular risk factors through lifestyle modifications, and prescription of drugs for primary or secondary prevention. Which examinations are necessary, and when do they have to be scheduled? How often should a TKI-treated patient undergo wh…

0301 basic medicineOncologycardiovascular riskmedicine.medical_specialtychronic myelocytic leukemiacardio-oncologyPhysiologyReviewSettore MED/15 - Malattie Del Sangue03 medical and health sciencescardiovascular events0302 clinical medicineInternal medicinePhysiology (medical)hemic and lymphatic diseasesmedicineNeoplasmQP1-981Medical prescriptionAdverse effectMyeloproliferative neoplasmHematologyMechanism (biology)business.industryMyeloid leukemiamedicine.diseaseSettore MED/11 - Malattie Dell'Apparato Cardiovascolarerespiratory tract diseasestyrosine kinase inhibitions therapy030104 developmental biology030220 oncology & carcinogenesiscardiovascular events chronic myelocytic leukemia cardiovascular risk cardio-oncology tyrosine kinase inhibitions therapybusinessTyrosine kinaseFrontiers in Physiology
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Beyond evidence-based data: Scientific rationale and tumor behavior to drive sequential and personalized therapeutic strategies for the treatment of …

2016

The recent advances in identification of the molecular mechanisms related to tumorigenesis and angiogenesis, along with the understanding of molecular alterations involved in renal cell carcinoma (RCC) pathogenesis, has allowed the development of several new drugs which have revolutionized the treatment of metastatic renal cell carcinoma (mRCC). This process has resulted in clinically significant improvements in median overall survival and an increasing number of patients undergoes two or even three lines of therapy. Therefore, it is necessary a long-term perspective of the treatment: planning a sequential and personalized therapeutic strategy to improve clinical outcome, the potential to a…

0301 basic medicineOncologymedicine.medical_specialtyEvidence-based practicemedicine.drug_classSettore MED/06 - Oncologia MedicaVEGF receptorsAntineoplastic AgentsReviewurologic and male genital diseasesrenal cell cancerTyrosine-kinase inhibitor03 medical and health sciencesangiogenesis0302 clinical medicinetyrosine kinase inhibitorQuality of lifeRenal cell carcinomaInternal medicineAngiogenesis; MTOR; Renal cell cancer; Tyrosine kinase inhibitor; VEGFr; OncologymedicineOverall survivalAnimalsHumansMolecular Targeted TherapyPrecision MedicineCarcinoma Renal CellTherapeutic strategybiologybusiness.industryPrecision medicinemedicine.diseaseKidney NeoplasmsSurgeryAngiogenesiSettore MED/18 - Chirurgia GeneraleVEGFr030104 developmental biologyOncology030220 oncology & carcinogenesisbiology.proteinmTORbusiness
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Personalization of regorafenib treatment in metastatic gastrointestinal stromal tumours in real-life clinical practice

2017

Background: Regorafenib (REG) has now been approved as the standard third-line therapy in metastatic gastrointestinal stromal tumour (GIST) patients at the recommended dose and schedule of 160 mg once daily for the first 3 weeks of each 4-week cycle. However, it has a relevant toxicity profile that mainly occurs within the first cycles of therapy, and dose and schedule adjustments are often required to reduce the frequency or severity of adverse events and to avoid early treatment discontinuation. To date, large amounts of data on the use of REG in metastatic GIST patients in daily clinical practice are not available, and we lack information about how this treatment personalization really a…

0301 basic medicineOncologymedicine.medical_specialtyScheduleStromal cellSettore MED/06 - Oncologia Medicalcsh:RC254-282PersonalizationNO03 medical and health scienceschemistry.chemical_compound0302 clinical medicinetyrosine kinase inhibitorQuality of lifeInternal medicineRegorafenibtyrosine kinase inhibitorsmedicineOriginal Researchreferral centresGiSTbusiness.industryGIST; personalized treatment; quality of life; referral centres; regorafenib; tyrosine kinase inhibitors; OncologyGastrointestinal stromal tumourslcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogenspersonalized treatmentClinical PracticeGIST; personalized treatment; quality of life; referral centres; regorafenib; tyrosine kinase inhibitorsreferral centre030104 developmental biologychemistryquality of lifeOncology030220 oncology & carcinogenesisregorafenibbusinessGIST personalized treatment quality of life referral centres regorafenib tyrosine kinase inhibitorsGIST
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A narrative review of MET inhibitors in non-small cell lung cancer with MET exon 14 skipping mutations

2021

Treatment of advanced non-small cell lung cancer (NSCLC) has radically improved in the last years due to development and clinical approval of highly effective agents including immune checkpoint inhibitors (ICIs) and oncogene-directed therapies. Molecular profiling of lung cancer samples for activated oncogenes, including epidermal growth factor receptor (EGFR), anaplastic lymphoma kinase (ALK), c-ros oncogene 1 (ROS1) and BRAF, is routinely performed to select the most appropriate up-front treatment. However, the identification of new therapeutic targets remains a high priority. Recently, MET exon 14 skipping mutations have emerged as novel actionable oncogenic alterations in NSCLC, sensiti…

0301 basic medicineOncologymedicine.medical_specialtybiologybusiness.industryCancernon-small cell lung cancer (NSCLC)medicine.disease03 medical and health sciencesExon030104 developmental biology0302 clinical medicineOncology030220 oncology & carcinogenesisInternal medicineROS1biology.proteinMET; MET exon 14 skipping mutations; MET-tyrosine kinase inhibitors (TKIs); Non-small cell lung cancer (NSCLC)MedicineAnaplastic lymphoma kinaseEpidermal growth factor receptorbusinessLung cancerTyrosine kinase
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Chemoresistance and chemosensitization in cholangiocarcinoma

2017

One of the main difficulties in the management of patients with advanced cholangiocarcinoma (CCA) is their poor response to available chemotherapy. This is the result of powerful mechanisms of chemoresistance (MOC) of quite diverse nature that usually act synergistically. The problem is often worsened by altered MOC gene expression in response to pharmacological treatment. Since CCA includes a heterogeneous group of cancers their genetic signature coding for MOC genes is also diverse; however, several shared traits have been defined. Some of these characteristics are shared with other types of liver cancer, namely hepatocellular carcinoma and hepatoblastoma. An important goal in modern onco…

0301 basic medicinePharmacologybile ductschemotherapydrug delivery systems0302 clinical medicineChemosensitizationantineoplastic agentsmolecular biologyReceptorhumansreceptor protein-tyrosine kinasesmedia_commonapoptosisgene expression regulationbile duct neoplasmsDrug Resistance Multipletargeted therapiesGene Expression Regulation Neoplasticmultiplebiliary cancer; chemotherapy; liver cancer; multidrug resistance; targeted therapies; antineoplastic agents; apoptosis; bile duct neoplasms; bile ducts; cell survival; cholangiocarcinoma; drug delivery systems; drug resistance multiple; drug resistance; neoplasm; epithelial cells; gene expression regulation neoplastic; genetic therapy; humans; protein kinase inhibitors; receptor protein-tyrosine kinases; signal transduction; treatment outcome; molecular medicine; molecular biology030220 oncology & carcinogenesisHepatocellular carcinomabiliary cancerLiver cancercholangiocarcinomaTyrosine kinasesignal transductionDrugHepatoblastomamedia_common.quotation_subjectcell survivalPharmacological treatmentliver cancer03 medical and health sciencesmultidrug resistancemedicinemolecular medicinedrug resistancebusiness.industrymedicine.diseaseepithelial cellsneoplasticprotein kinase inhibitors030104 developmental biologyDrug Resistance NeoplasmCancer researchtreatment outcomebusinessneoplasmgenetic therapy
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Prognostic use of soluble fms-like tyrosine kinase-1 and placental growth factor in patients with coronary artery disease.

2015

Background: Intention of the study is to assess the cardiovascular mortality of patients with coronary artery disease (CAD) with the biomarkers of angiogenesis PlGF and its endogenous inhibitor sFlt-1. Methods: The cohort included n = 1848 patients with CAD and 282 subjects without CAD. In 85 patients cardiovascular mortality, as combination of fatal myocardial infarction or any cardiac death, during a median follow-up duration of 3.9 years was reported. Results: In Kaplan–Meier curve analysis PlGF in rising thirds was not predictive regarding outcome (p = 0.54), the same was shown for sFlt-1 (p = 0.44). Cox regression for the fully adjusted model provided a hazard ratio (HR) of 0.8 (p = 0…

0301 basic medicinePlacental growth factorMalemedicine.medical_specialtyClinical BiochemistryCoronary Artery DiseaseKaplan-Meier Estimate030204 cardiovascular system & hematologyPregnancy ProteinsCoronary artery disease03 medical and health scienceschemistry.chemical_compound0302 clinical medicineInternal medicineDrug DiscoveryNatriuretic Peptide BrainmedicineHumansMyocardial infarctionPlacenta Growth FactorVascular Endothelial Growth Factor Receptor-1Proportional hazards modelbusiness.industryBiochemistry (medical)Hazard ratioMiddle Agedmedicine.diseasePrognosisPeptide FragmentsVascular endothelial growth factor030104 developmental biologyEndocrinologychemistryCohortCardiologyFemalebusinessSoluble fms-like tyrosine kinase-1Follow-Up StudiesBiomarkers in medicine
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SWATH-MS based quantitative proteomics analysis reveals that curcumin alters the metabolic enzyme profile of CML cells by affecting the activity of m…

2018

Background Chronic myelogenous leukemia (CML) is a myeloproliferative disorder caused by expression of the chimeric BCR-ABL tyrosine kinase oncogene, resulting from the t(9;22) chromosomal translocation. Imatinib (gleevec, STI-571) is a selective inhibitor of BCR-ABL activity highly effective in the treatment of CML. However, even though almost all CML patients respond to treatment with imatinib or third generation inhibitors, these drugs are not curative and need to be taken indefinitely or until patients become resistant. Therefore, to get a definitive eradication of leukemic cells, it is necessary to find novel therapeutic combinations, for achieving greater efficacy and fewer side effec…

0301 basic medicineProteomicsCancer ResearchCurcuminCML cellsCellReceptors Cytoplasmic and NuclearKaryopherinsTransfectionlcsh:RC254-282Mass SpectrometrymiR-22/IPO7/HIF-1α axis03 medical and health scienceschemistry.chemical_compound0302 clinical medicinemiR-22/IPO7/HIF-1α axiSettore BIO/13 - Biologia Applicatahemic and lymphatic diseasesCell Line TumorLeukemia Myelogenous Chronic BCR-ABL PositivemedicineHumansCML cells; Curcumin; miR-22/IPO7/HIF-1α axis; SWATH-MS; Oncology; Cancer ResearchOncogeneChemistryResearchCML cellImatinibTransfectionmedicine.diseaseHypoxia-Inducible Factor 1 alpha Subunitlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens3. Good healthMicroRNAs030104 developmental biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesisCancer researchCurcuminSWATH-MSK562 CellsTyrosine kinaseK562 cellsChronic myelogenous leukemiamedicine.drug
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