Search results for "TYROSINE KINASE INHIBITOR"

showing 10 items of 50 documents

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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Gut microbiota and cancer: How gut microbiota modulates activity, efficacy and toxicity of antitumoral therapy

2019

Gut microbiota is involved in gastrointestinal carcinogenesis. Also, it modulates the activity, efficacy and toxicity of several chemotherapy agents, such as gemcitabine, cyclophosphamide, irinotecan, cisplatin and 5-Fluorouracil, and target therapy, such as tyrosine kinase inhibitors. More recently, accumulating data suggest that the composition of gut microbiota may also affect efficacy and toxicity of cancer immunotherapy. Therefore, the manipulation of gut microbiota through antibiotics, probiotics, prebiotics or fecal transplantation has been investigating with the aim to improve efficacy and mitigate toxicity of anticancer drugs.

0301 basic medicineSettore MED/06 - Oncologia Medicamedicine.drug_class5-Fluorouracilmedicine.medical_treatmentAntibioticsAntineoplastic AgentsImmune checkpoint inhibitorGut floraPharmacologyIrinotecandigestive systemImmune checkpoint inhibitors03 medical and health sciences0302 clinical medicineCancer immunotherapyNeoplasmsmedicineAnimalsHumansCyclophosphamide5-Fluorouracil; Cisplatin; Cyclophosphamide; Gemcitabine; Immune checkpoint inhibitors; Irinotecan; Microbiota; Tyrosine kinase inhibitorsTyrosine kinase inhibitorsChemotherapybiologybusiness.industryMicrobiotaCancerHematologyFecal Microbiota Transplantationbiology.organism_classificationmedicine.diseaseGemcitabineGemcitabineGastrointestinal MicrobiomeIrinotecan030104 developmental biologyOncology030220 oncology & carcinogenesisToxicityImmunotherapyCisplatinbusinessmedicine.drugCritical Reviews in Oncology/Hematology
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Osteonecrosis of the jaw related to non-antiresorptive medications: a systematic review

2018

The reporting of osteonecrosis of the jaw (ONJ) related to anticancer agents without known antiresorptive properties (non-antiresorptives), such as antiangiogenics, tyrosine kinase inhibitors, mammalian target of rapamycin inhibitors, immune checkpoint inhibitors, and cytotoxic chemotherapy is increasing. To review characteristics of ONJ in cancer patients receiving non-antiresorptives. A systematic review of the literature between 2009 and 2017 was conducted by the Bone Study Group of MASCC/ISOO. Of 6249 articles reviewed and from personal communication, 42 ONJ cases related to non-antiresorptives were identified. No gender predilection was noted. Median age was 60 years and ONJ stage 2 wa…

AdultMaleOncologyBRAF inhibitormedicine.medical_specialtymTOR inhibitorsImmune checkpoint inhibitorsInhibitors of angiogenesiTyrosine kinase inhibitorBone resorptionImmune checkpoint inhibitorDelayed diagnosisCytotoxic chemotherapyBone resorption03 medical and health sciences0302 clinical medicineProstateInternal medicinemedicineHumans030212 general & internal medicineStage (cooking)AgedBone Density Conservation AgentsDiphosphonatesOsteonecrosis of the jawbusiness.industryOsteonecrosisCancerMiddle AgedCytotoxic chemotherapymedicine.diseasemedicine.anatomical_structureJawOncology030220 oncology & carcinogenesisBisphosphonate-Associated Osteonecrosis of the JawFemaleOsteonecrosis of the jawbusiness
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Late onset of unilateral optic disk edema secondary to treatment with imatinib mesylate

2017

Key Clinical Message Prompt ophthalmology evaluation and immediate imatinib suspension should be suggested at any time of tyrosine kinase inhibitor therapy in patients with visual deficit, as it may be a clinical manifestation of optic disk edema, and suspension may help in prompt recovery.

Adverse event0301 basic medicinegenetic structuresmedicine.drug_classOptic Disk EdemaLate onsetCase ReportClinical manifestationCase ReportsTyrosine-kinase inhibitor03 medical and health sciences0302 clinical medicinechronic myeloid leukemiatyrosine kinase inhibitorsmedicineIn patientAdverse effectbusiness.industryoptic disk edemaImatinibGeneral Medicineeye diseases030104 developmental biologyImatinib mesylateimatiniboptic nerve edemaAnesthesiaAdverse events030221 ophthalmology & optometrybusinessmedicine.drugClinical Case Reports
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A recommended practical approach to the management of target therapy and angiogenesis inhibitors cardiotoxicity: an opinion paper of the working grou…

2016

The US National Cancer Institute estimates that cardiotoxicity (CTX) from target therapy refers mostly to four groups of drugs: epidermal growth factor receptor 2 inhibitors, angiogenic inhibitors, directed Abelson murine leukemia viral oncogene homolog inhibitors, and proteasome inhibitors. The main cardiotoxic side-effects related to antiepidermal growth factor receptor 2 therapy are left ventricular systolic dysfunction and heart failure. Angiogenesis inhibitors are associated with hypertension, left ventricular dysfunction/heart failure, myocardial ischemia, QT prolongation, and thrombosis. Moreover, other agents may be related to CTX induced by treatment. In this study, we review the g…

AngiogenesisLeftAngiogenesis Inhibitors030204 cardiovascular system & hematologyVentricular Dysfunction Left0302 clinical medicinetyrosine kinase inhibitorNeoplasmstyrosine kinase inhibitorsVentricular DysfunctionMolecular Targeted TherapyEpidermal growth factor receptorSocieties Medicalangiogenesis inhibitors; HER2/epidermal growth factor receptor 2; tyrosine kinase inhibitorABLbiologyDisease ManagementGeneral MedicineItalyCardiovascular DiseasesSupplement Submission030220 oncology & carcinogenesisangiogenesis inhibitors; HER2/epidermal growth factor receptor 2; tyrosine kinase inhibitors; Angiogenesis Inhibitors; Antineoplastic Agents; Cardiology; Cardiomyopathies; Cardiotoxicity; Heart Failure; Humans; Italy; Neoplasms; Practice Guidelines as Topic; Societies Medical; Ventricular Dysfunction Left; Disease ManagementPractice Guidelines as TopicCardiologyCardiology and Cardiovascular MedicineCardiomyopathiesmedicine.medical_specialtyCardiologyAntineoplastic AgentsRisk AssessmentQT interval03 medical and health sciencesGrowth factor receptorInternal medicineMedicalmedicineHumansMonitoring PhysiologicHeart FailureCardiotoxicitybusiness.industryCancerHER2/epidermal growth factor receptor 2medicine.diseaseangiogenesis inhibitors; HER2/epidermal growth factor receptor 2; tyrosine kinase inhibitors; Cardiology and Cardiovascular MedicineCardiotoxicityangiogenesis inhibitorHeart failurebiology.proteinbusinessSocietiesJournal of cardiovascular medicine (Hagerstown, Md.)
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Tyrosine Kinase Inhibitors for the Treatment of Chronic Myeloid Leukemia

2009

Imatinib mesylate (Gleevec) is a drug unique for the treatment of certain forms of cancer. It works by targeting, and turning off, specific tyrosine kinase proteins that cause the uncontrolled cell growth and the inhibition of apoptosis in cancer cells. Imatinib was designed on the basis of the structure of the ATP binding site of the Abl protein kinase with the aim to stabilizes the inactive form of Bcr-Abl, an oncoprotein involved in malignant transformation in chronic myelogenous leukemia (CML). However, imatinib can also target other tyrosine kinase proteins different from Bcr-Abl such as Kit, that is the suspected cause of gastrointestinal stromal tumor (GIST). Despite successful clini…

Cancer ResearchFusion Proteins bcr-ablAntineoplastic AgentsApoptosisPharmacologyhemic and lymphatic diseasesLeukemia Myelogenous Chronic BCR-ABL PositivemedicineHumansProtein kinase AneoplasmsProtein Kinase InhibitorsPharmacologyTyrosine kinase inhibitorsABLbusiness.industryBcr-Abl chronic myelogenous leukemia tyrosine kinase inhibitorsMyeloid leukemiaImatinibProtein-Tyrosine Kinasesmedicine.diseaseBcr-Abl; Chronic myelogenous leukemia; Tyrosine kinase inhibitors;LeukemiaImatinib mesylateCancer researchMolecular MedicinebusinessTyrosine kinaseChronic myelogenous leukemiamedicine.drugChronic myelogenous leukemiaBcr-Abl
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The new iodoacetamidobenzofuran derivative TR120 decreases STAT5 expression and induces antitumor effects in imatinib-sensitive and imatinib-resistan…

2013

The identification of novel compounds modulating the expression/activity of molecular targets downstream to BCR-ABL could be a new approach in the treatment of chronic myeloid leukemias (CMLs) resistant to imatinib or other BCR-ABL-targeted molecules. Recently, we synthesized a new class of substituted 2-(3,4,5-trimethoxybenzoyl)-2-N,N-dimethylamino-benzo[b]furans, and among these 3-iodoacetylamino-6-methoxybenzofuran-2-yl(3,5-trimethoxyphenyl)methanone (TR120) showed marked cytotoxic activity in BCR-ABL-expressing cells. Interestingly, TR120 was more potent than imatinib in cell growth inhibition and apoptosis induction in both BCR-ABL-expressing K562 and KCL22 cells. Moreover, it showed a…

Cancer ResearchFusion Proteins bcr-ablApoptosisPiperazinesSettore MED/15 - Malattie Del Sanguechemistry.chemical_compoundhemic and lymphatic diseasesSTAT5 Transcription FactorCytotoxic T cellPharmacology (medical)Cyclin D1STAT5biologyDrug SynergismCell cycleNeoplasm ProteinsGene Expression Regulation NeoplasticLeukemiaOncologyProto-Oncogene Proteins c-bcl-2BenzamidesImatinib MesylateGrowth inhibitionmedicine.drugbcl-X ProteinDown-RegulationAntineoplastic AgentsBone Marrow CellsResting Phase Cell CycleColony-Forming Units AssayBenzophenonesNecrosisCell Line TumorLeukemia Myelogenous Chronic BCR-ABL PositivemedicineHumansneoplasmsBenzofuransPharmacologyG1 PhaseImatinibBCR-ABL chronic myeloid leukemia imatinib resistance STAT5 tyrosine kinase inhibitorsmedicine.diseaseSettore CHIM/08 - Chimica FarmaceuticaGenes bcl-1Genes bcl-2PyrimidineschemistryApoptosisDrug Resistance NeoplasmSettore BIO/14 - FarmacologiaCancer researchbiology.proteinK562 CellsK562 cells
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Tumor-intrinsic and -extrinsic roles of c-Kit: mast cells as the primary off-target of tyrosine kinase inhibitors.

2011

c-Kit tyrosine kinase receptor and its ligand stem cell factor have multiple functions during development, whereas in adulthood they are mostly needed for stem cell (SC) maintenance and mast cell (MC) biology. c-Kit plays an essential tumor-cell-intrinsic role in many types of cancer, either providing the tumorigenic force when aberrantly activated or conferring stem-like features characterizing the most aggressive variants. A tumor-cell-extrinsic role occurs through c-Kit-dependent accessory cells (such as MCs) that infiltrate tumors and deeply influence their progression. c-Kit-targeted therapy with tyrosine kinase inhibitors (TKIs) may ideally work against both tumor and stromal cells. H…

Cancer ResearchStromal cellStem cell factorAntineoplastic AgentsBiologyc-kit; mast cells; mouse mutants; off-target; tyrosine kinase inhibitorsReceptor tyrosine kinaseMicec-KitNeoplasmstyrosine kinase inhibitorsGeneticsmedicineAnimalsHumansNeoplasm InvasivenessMast CellsMolecular BiologyProtein Kinase InhibitorsStem Cell Factormouse mutantsNeovascularization PathologicMast cellRatsProto-Oncogene Proteins c-kitmedicine.anatomical_structureTumor progressionmast cells.biology.proteinCancer researchStem cellTyrosine kinasePlatelet-derived growth factor receptoroff-targetMastocytosisOncogene
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Phase 0/1 of Positron Emission Tomography (PET) imaging agent [18F]-ODS2004436 as a marker of EGFR mutation in patients with non-small cell lung canc…

2018

e24184Background: Multiple EGFR tyrosine kinase inhibitors (TKIs) are approved for treatment of NSCLC harboring EGFR activating mutations or secondary TKIs resistant mutation. We evaluate a new PET...

Cancer Research[SDV.IB.IMA]Life Sciences [q-bio]/Bioengineering/Imagingnon-small cell lung cancer (NSCLC)[SDV.IB.MN]Life Sciences [q-bio]/Bioengineering/Nuclear medicine[SDV.IB.MN] Life Sciences [q-bio]/Bioengineering/Nuclear medicine03 medical and health sciences0302 clinical medicinemedicineIn patientComputingMilieux_MISCELLANEOUSmedicine.diagnostic_testbusiness.industryPet imagingmedicine.diseaseEGFR Tyrosine Kinase Inhibitorsrespiratory tract diseases3. Good health[SDV.IB.IMA] Life Sciences [q-bio]/Bioengineering/ImagingOncologyEgfr mutationPositron emission tomography030220 oncology & carcinogenesisMutation (genetic algorithm)Cancer researchbusiness030215 immunology
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