Search results for " tyrosine kinase inhibitors"

showing 10 items of 31 documents

Observational study of chronic myeloid leukemia Italian patients who discontinued tyrosine kinase inhibitors in clinical practice.

2018

It is judged safe to discontinue treatment with tyrosine kinase inhibitors (TKI) for chronic myeloid leukemia (CML) in experimental trials on treatment-free remission (TFR). We collected a total of 293 Italian patients with chronic phase CML who discontinued TKI in deep molecular response. Seventy-two percent of patients were on treatment with imatinib, and 28% with second generation TKI at the time of discontinuation. Median duration of treatment with the last TKI was 77 months [Interquartile Range (IQR) 54;111], median duration of deep molecular response was 46 months (IQR 31;74). Duration of treatment with TKI and duration of deep molecular response were shorter with second generation TK…

MaleImatinib mesylate discontinuation; chronic myelogenous leukemia; treatment-free remission; long-term outcomes; molecular response; cml patients; recommendations; management; dasatinib; cessationchemistry.chemical_compound0302 clinical medicineTreatment Free RemissionPregnancyMED/15 - MALATTIE DEL SANGUEInterquartile rangeingleseMedicinedasatinibChronic Myelogenous Leukemiatreatment-free remissionPonatinibmolecular responseHematologyMiddle AgedProtein-Tyrosine Kinasescml patientsDasatinibTreatment OutcomeLeukemia Myeloid Chronic-PhaseDisease ProgressionImatinib MesylateFemaleChronic Myelogenous Leukemia; Discontinuation; Treatment Free Remissionlong-term outcomesmanagementmedicine.drugAdultmedicine.medical_specialtyChronic Myeloid LeukemiaSocio-culturaleDiscontinuationArticletyrosine kinase inhibitors discontinued treatment chronic myeloid leukemia treatment-free remission (TFR)Safety-Based Drug Withdrawals03 medical and health scienceschronic myeloid leukemia tyrosine kinase inhibitors discontinuationMedian follow-upLeukemia Myelogenous Chronic BCR-ABL PositiveInternal medicineImatinib mesylate discontinuationHumansProtein Kinase InhibitorsRetrospective Studiesbusiness.industryImatinibmedicine.diseaseDiscontinuationrespiratory tract diseasesSettore MED/15 - MALATTIE DEL SANGUEcessationNilotinibchemistryrecommendationsbusiness030215 immunologyChronic myelogenous leukemia
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Differences among young adults, adults and elderly chronic myeloid leukemia patients

2014

Abstract BACKGROUND: The incidence of chronic myeloid leukemia (CML) increases with age, but it is unclear how the characteristics of the disease vary with age. In children, where CML is very rare, it presents with more aggressive features, including huge splenomegaly, higher cell count and higher blast cell percentage. PATIENTS AND METHODS: To investigate if after childhood the disease maintains or loses these characteristics of aggressiveness, we analyzed 2784 adult patients, at least 18 years old, registered by GIMEMA CML WP over a 40-year period. RESULTS: Young adults (YAs: 18-29 years old) significantly differed from adults (30-59 years old) and elderly patients (at least 60 years old)…

MalePediatricsHost responseBCR-ABL; Chronic myeloid leukemia; Prognosis; Tyrosine kinase inhibitors; Young adults; Adult; Age Factors; Aged; Aged 80 and over; Antineoplastic Agents; Female; Humans; Leukemia Myelogenous Chronic BCR-ABL Positive; Male; Middle Aged; Prospective Studies; Protein Kinase Inhibitors; Protein-Tyrosine Kinases; Spleen; Splenomegaly; Young Adult; Oncology; HematologyTyrosine kinase inhibitorDiseaseAntineoplastic AgentTyrosin kinase inhibitorProtein-Tyrosine Kinasehemic and lymphatic diseases80 and overAge FactorProspective StudiesYoung adultChronicBCR-ABLAged 80 and overLeukemiaIncidence (epidemiology)Chronic myeloid leukemiaAge FactorsMyeloid leukemiaHematologyMiddle AgedProtein-Tyrosine KinasesPrognosisLeukemiaOncologybcr-abl1FemaleBCR-ABL; chronic myeloid leukemia; prognosis; tyrosine kinase inhibitors; young adultsHumanAdultyoung adultsmedicine.medical_specialtyPrognosiProtein Kinase InhibitorAntineoplastic Agentschronic myeloid leukemia; bcr-abl1; Tyrosin kinase inhibitor; prognosis; young adultsNOYoung Adultchronic myeloid leukemiaLeukemia Myelogenous Chronic BCR-ABL PositivemedicineHumansBCR-ABL; Chronic myeloid leukemia; Prognosis; Tyrosine kinase inhibitors; Young adults; Adult; Age Factors; Aged; Aged 80 and over; Antineoplastic Agents; Female; Humans; Leukemia Myelogenous Chronic BCR-ABL Positive; Male; Middle Aged; Prospective Studies; Protein Kinase Inhibitors; Protein-Tyrosine Kinases; Spleen; Splenomegaly; Young AdultProtein Kinase InhibitorsAgedTyrosine kinase inhibitorsAdult patientsbusiness.industrymedicine.diseaseClinical trialBCR-ABL; Chronic myeloid leukemia; Prognosis; Tyrosine kinase inhibitors; Young adults; Adult; Age Factors; Aged; Aged 80 and over; Antineoplastic Agents; Female; Humans; Leukemia Myelogenous Chronic BCR-ABL Positive; Male; Middle Aged; Prospective Studies; Protein Kinase Inhibitors; Protein-Tyrosine Kinases; Spleen; Splenomegaly; Young Adult; Hematology; OncologyProspective StudieBCR-ABL; Chronic myeloid leukemia; Prognosis; Tyrosine kinase inhibitors; Young adults; Adult; Age Factors; Aged; Aged 80 and over; Antineoplastic Agents; Female; Humans; Leukemia Myelogenous Chronic BCR-ABL Positive; Male; Middle Aged; Prospective Studies; Protein Kinase Inhibitors; Protein-Tyrosine Kinases; Spleen; Splenomegaly; Young Adult; Medicine (all); Hematology; OncologyImmunologySplenomegalyBCR-ABL PositiveBCR-ABL chronic myeloid leukemia prognosis tyrosine kinase inhibitors young adultsprognosisbusinessSpleenYoung adultsMyelogenous
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Stereotactic Radiotherapy for the Treatment of Patients With Oligo-progressive Metastatic Renal Cell Carcinoma Receiving Vascular Endothelial Growth …

2020

Aim This retrospective observational study evaluated the role of hypo-fractionated stereotactic radiotherapy (SRT) in patients with oligo-progressive metastatic renal cell carcinoma (mRCC) treated with first-line oral tyrosine kinase inhibitors (TKI). Data on local control, delay of further progression, and safety are reported. Patients and methods Between January 2010 and December 2016, 28 patients with mRCC who showed oligo-progressive disease while receiving first-line pazopanib were treated with hypofractionated SRT to progressive metastatic sites to delay the change of systemic therapy. First and second progression-free survival (PFS-1 and PFS-2) were recorded, as well as objective res…

OncologyAdultMaleCancer Researchmedicine.medical_specialtymedicine.drug_classmedicine.medical_treatmentTyrosine-kinase inhibitorDisease-Free SurvivalMetastasisPazopanibRenal cell carcinomaInternal medicinetyrosine kinase inhibitorsmedicinepazopanibmetastasisHumansNeoplasm MetastasisCarcinoma Renal CellProtein Kinase InhibitorsAgedRetrospective Studiesbusiness.industryCarcinomaRenal CellRetrospective cohort studyGeneral MedicineMiddle Agedmedicine.diseasemetastasis; pazopanib; Renal cell carcinoma; stereotactic radiotherapy; tyrosine kinase inhibitors; Adult; Aged; Carcinoma Renal Cell; Disease-Free Survival; Female; Humans; Kidney Neoplasms; Male; Middle Aged; Neoplasm Metastasis; Protein Kinase Inhibitors; Retrospective StudiesRenal cell carcinomaKidney NeoplasmsRadiation therapyOncologyToxicitystereotactic radiotherapyFemalebusinessTyrosine kinasemedicine.drug
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High-dose radiotherapy for oligo-progressive NSCLC receiving EGFR tyrosine kinase inhibitors: Real world data

2020

Background/aim Local ablative treatments for oligo-progressive, EGFR mutated non-small cell lung cancer (mut-NCSLC) may improve long-term disease control and survival. We analyzed the efficacy of hypo-fractionated, high-dose radiation therapy (HDRT), in association with prolonged EGFR tyrosine kinase inhibitors (TKI) in oligo-progressive, EGFR mutant-NSCLC. Patients and methods Progression-free survival-1 (PFS-1, date from initiation of TKI therapy until oligo-progression or death), and progression-free survival-2 (PFS-2, date of focal progression until further progression or death) were evaluated. Results Thirty-six patients were analyzed. The median PFS 1 was 12.5 months. HDHRT consisted …

OncologyCancer Researchmedicine.medical_specialtyLung Neoplasmsmedicine.medical_treatmentEGFR high-dose radiotherapy Non-small cell lung cancer oligo-progressionEGFRGeneral Biochemistry Genetics and Molecular Biologyoligo-progression03 medical and health sciences0302 clinical medicineNon-small cell lung cancerCarcinoma Non-Small-Cell LungInternal medicinemedicineOverall survivalHumansProtein Kinase InhibitorsRetrospective StudiesPharmacologybusiness.industryEGFR Non-small cell lung cancer high-dose radiotherapy oligo-progressionEGFR; High-dose radiotherapy; Non-small cell lung cancer; Oligo-progressionEGFR Tyrosine Kinase Inhibitorshigh-dose radiotherapyDisease controlProgression-Free SurvivalErbB ReceptorsRadiation therapy030220 oncology & carcinogenesisMutationNon small cellbusinessReal world dataResearch Article
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Real-Life Clinical Data of Cabozantinib for Unresectable Hepatocellular Carcinoma

2021

<b><i>Introduction:</i></b> Cabozantinib has been approved by the European Medicine Agency (EMA) for hepatocellular carcinoma (HCC) previously treated with sorafenib. Cabozantinib is also being tested in combination with immune checkpoint inhibitors in the frontline setting. Real-life clinical data of cabozantinib for HCC are still lacking. Moreover, the prognostic factors for HCC treated with cabozantinib have not been investigated. <b><i>Methods:</i></b> We evaluated clinical data and outcome of HCC patients who received cabozantinib in the legal context of named patient use in Italy. <b><i>Results:</i></b> Ninety-six…

OncologySorafenibmedicine.medical_specialtyCabozantinibHepatocellular carcinomaContext (language use)chemistry.chemical_compoundInternal medicineCabozantinib; Hepatocellular carcinoma; Outcome; Sorafenib; Tyrosine kinase inhibitorsmedicineAdverse effectRC254-282OutcomeTyrosine kinase inhibitorsSettore MED/12 - GastroenterologiaOriginal PaperHepatologyPerformance statusbusiness.industryNeoplasms. Tumors. Oncology. Including cancer and carcinogensCabozantinibSorafenibmedicine.diseaseClinical trialOncologychemistryHepatocellular carcinomaLiver functionbusinessmedicine.drug
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Early diagnosis, clinical management, and follow-up of cardiovascular events with ponatinib

2020

Chronic myeloid leukemia (CML) is a myeloproliferative disorder characterized by neoplastic transformation of pluripotent cells due to a typical cytogenetic and molecular mutation known as Philadelphia (Ph) chromosome. In 2001, the introduction of the tyrosine kinasis inhibitor (TKI) imatinib as a therapeutic strategy for CML with PH chromosome mutation represented an important step towards treatment of these patients, and nowadays, this drug represents the gold therapeutic standard in this clinical setting. A second generation of TKIs (dasatinib, nilotinib, and bosutinib) showed an effective action in all patients with mutations resistant to imatinib. Ponatinib is a third-generation TKI an…

Oncologymedicine.medical_specialtyTyrosine kinase inhibitorReview030204 cardiovascular system & hematology03 medical and health scienceschemistry.chemical_compound0302 clinical medicineRisk FactorsLeukemia Myelogenous Chronic BCR-ABL Positivehemic and lymphatic diseasesInternal medicinemedicineHumansNeoplastic transformation030212 general & internal medicineProtein Kinase InhibitorsTyrosine kinase inhibitorsCardiotoxicitybusiness.industryPonatinibChronic myeloid leukemiaImidazolesDisease ManagementMyeloid leukemiaImatinibPyridazinesDasatinibCardio-oncologyEarly DiagnosisNilotinibchemistryCardiovascular DiseasesPonatinibPonatinib . Tyrosine kinase inhibitors . Chronic myeloid leukemia . Cardio-oncology . ReviewCardiology and Cardiovascular MedicinebusinessBosutinibFollow-Up Studiesmedicine.drug
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Sodium-glucose cotransporter type 2 inhibitors prevent ponatinib-induced endothelial senescence and disfunction: A potential rescue strategy

2021

Background: Ponatinib (PON), a third-generation tyrosine kinase inhibitor (TKI), has proven cardiovascular toxicity, with no known preventing agents usable to limit such side effect. Sodium-glucose cotransporter type 2 (SGLT2) inhibitors are a new class of glucose-lowering agents, featuring favorable cardiac and vascular effects. Aims: We assessed the effects of the SGLT2 inhibitors empagliflozin (EMPA) and dapagliflozin (DAPA) on human aortic endothelial cells (HAECs) and underlying vasculo-protective mechanisms in an in vitro model of PON-induced endothelial toxicity. Methods and results: We exposed HAECs to PON or vehicle (DMSO) in the presence or absence of EMPA (100 and 500 nmol/L) or …

Physiologymedicine.drug_classCellPharmacologyAutophagy; Ponatinib; Sodium-glucose cotransporter type 2 (SGLT2) inhibitors; Tyrosine kinase inhibitors; Vascular toxicityTyrosine-kinase inhibitorFlow cytometrychemistry.chemical_compoundmedicineAutophagyHumansViability assayDapagliflozinCellular SenescencePharmacologyTyrosine kinase inhibitorsMatrigelmedicine.diagnostic_testChemistrySodiumImidazolesEndothelial CellsEndothelial stem cellPyridazinesmedicine.anatomical_structureGlucoseDiabetes Mellitus Type 2Sodium-glucose cotransporter type 2 (SGLT2) inhibitorsToxicityPonatinibMolecular MedicineVascular toxicity
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Antineoplastic Drug-Induced Cardiotoxicity: A Redox Perspective

2018

Antineoplastic drugs can be associated with several side effects, including cardiovascular toxicity (CTX). Biochemical studies have identified multiple mechanisms of CTX. Chemoterapeutic agents can alter redox homeostasis by increasing the production of reactive oxygen species (ROS) and reactive nitrogen species RNS. Cellular sources of ROS/RNS are cardiomyocytes, endothelial cells, stromal and inflammatory cells in the heart. Mitochondria, peroxisomes and other subcellular components are central hubs that control redox homeostasis. Mitochondria are central targets for antineoplastic drug-induced CTX. Understanding the mechanisms of CTX is fundamental for effective cardioprotection, without…

Stromal cellPhysiologymedicine.medical_treatmentTyrosine kinase inhibitorChemotherapy; HER-2 inhibitors; Oxidative/nitrosative stress; Tyrosine kinase inhibitors; Vascular endothelial growth factorReviewOxidative phosphorylation030204 cardiovascular system & hematologyMitochondrionPharmacologyChemotherapy; HER-2 inhibitors; Oxidative/nitrosative stress; Tyrosine kinase inhibitors; Vascular endothelial growth factor; Physiology; Physiology (medical)chemotherapyHER-2 inhibitorlcsh:Physiology03 medical and health scienceschemistry.chemical_compound0302 clinical medicinePhysiology (medical)tyrosine kinase inhibitorsMedicinechemotherapy HER-2 inhibitors oxidative/nitrosative stress vascular endothelial growth factor tyrosine kinase inhibitorsReactive nitrogen specieschemistry.chemical_classificationCardioprotectionReactive oxygen speciesChemotherapyCardiotoxicitylcsh:QP1-981vascular endothelial growth factorbusiness.industryOxidative/nitrosative strechemistry030220 oncology & carcinogenesisbusinessHER-2 inhibitorsoxidative/nitrosative stress
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Pretreatment T790M mutation detection by ultrasensitive PCR assay as predictor of efficacy in non-small lung cancer (NSCLC) patients treated with 1st…

2019

business.industryPcr assayHematologymedicine.diseaseEGFR Tyrosine Kinase Inhibitorslaw.inventionT790MOncologylawMutation (genetic algorithm)medicineCancer researchNon small lung cancerMutation detectionLung cancerbusinessPolymerase chain reactionAnnals of Oncology
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Nueva era en el combate contra el cáncer: Evolución y cáncer: progreso y tratamiento de tumores

2013

L’oncohematologia ha assistit en les últimes dècades a importants avenços en el tractament i supervivència. La toxicitat derivada de la quimioteràpia clàssica i la necessitat de millorar l’eficàcia i tolerància als tractaments han fet que es desencadene un allau d’activitat investigadora que constantment proporciona fruits. Gran part d’aquest esforç s’ha enfocat al desenvolupament de «teràpies diana» dirigides contra determinades alteracions funcionals, clau per a la supervivència de la cèl·lula tumoral. Així es pretén aconseguir major eficàcia en el tractament i que el pacient pague un menor cost en toxicitat. Avenços en altres disciplines de l’oncologia com l’epidemiologia, la cirurgia i …

evolucióncribado poblacionalmecanismes de resistènciafàrmacs antidianaresistance mechanismsbiologia; evolució; genèticaterapias dirigidas; fármacos anti diana; inhibidores tirosin kinasa; mecanismos de resistencia; cribado poblacionalevolutiontyrosine kinase inhibitorsteràpies dirigides; fàrmacs antidiana; inhibidors tirosina-cinasa; mecanismes de resistència; cribatge poblacionalinhibidores tirosin kinasageneticsteràpies dirigidesanti-target drugsbiologygenèticascreeningtargeted therapies; anti-target drugs; tyrosine kinase inhibitors; resistance mechanisms; screeningcribatge poblacionalmecanismos de resistenciatargeted therapiesevolución; biología; medicinaterapias dirigidasevoluciófármacos anti dianabiologíabiology; evolution; geneticsmedicinabiologiainhibidors tirosina-cinasa
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