Search results for "TYROSINE KINASE INHIBITOR"

showing 10 items of 50 documents

Gefitinib in lung cancer therapy. Clinical results, predictive markers of response and future perspectives.

2009

Over the past few years, epidermal growth factor receptor has emerged as one of the most important targets in tumorgenesis and several drugs targeting signal transduction pathways have been developed. The first among these agents to be approved for the treatment of NSCLC was gefitinib, a potent, selective and reversible inhibitor of HER1/EGFR tyrosine kinase activity. The review summarizes its clinical development and the new therapeutic options, with particular focus on predictive markers of susceptibility to this drug.

DrugOncologyCancer Researchmedicine.medical_specialtyLung Neoplasmsmolecular markersmedia_common.quotation_subjectgefitinibAntineoplastic AgentsGefitinibcancer therapyGefitinibCarcinoma Non-Small-Cell LungInternal medicinetyrosine kinase inhibitorsmedicineAnimalsHumansgefitinib; non-small cell lung cancer (NSCLC); epidermal growth factor receptor (HER1/EGFR); tyrosine kinase inhibitors; target therapy; molecular markers; EGFR mutationsEpidermal growth factor receptorLung cancermedia_commonPharmacologyClinical Trials as Topicbiologybusiness.industrytarget therapymedicine.diseaseEGFR mutationsepidermal growth factor receptor (HER1/EGFR)ErbB Receptorsnon-small cell lung cancer (NSCLC)OncologyQuinazolinesbiology.proteinMolecular MedicineSignal transductionbusinessBiomarkersEgfr tyrosine kinaseSignal Transductionmedicine.drug
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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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Genome-wide profiling of non-smoking-related lung cancer cells reveals common RB1 rearrangements associated with histopathologic transformation in EG…

2020

The etiology and the molecular basis of lung adenocarcinomas (LuADs) in nonsmokers are currently unknown. Furthermore, the scarcity of available primary cultures continues to hamper our biological understanding of non-smoking-related lung adenocarcinomas (NSK-LuADs). We established patient-derived cancer cell (PDC) cultures from metastatic NSK-LuADs, including two pairs of matched EGFR-mutant PDCs before and after resistance to tyrosine kinase inhibitors (TKIs), and then performed whole-exome and RNA sequencing to delineate their genomic architecture. For validation, we analyzed independent cohorts of primary LuADs. In addition to known non-smoker-associated alterations (e.g. RET, ALK, EGFR…

0301 basic medicineLung NeoplasmsEGFRUbiquitin-Protein LigasesAdenocarcinoma of Lungmedicine.disease_cause03 medical and health sciences0302 clinical medicineGermline mutationtyrosine kinase inhibitorsmedicineGenetic predispositionHumanswhole-exome sequencingLung cancerGeneProtein Kinase InhibitorsExome sequencingMutationbusiness.industryEGFR RB1 lung adenocarcinoma nonsmokers tyrosine kinase inhibitors whole-exome sequencingHematologyrespiratory systemmedicine.diseaselung adenocarcinomadigestive system diseasesrespiratory tract diseasesErbB ReceptorsRetinoblastoma Binding Proteins030104 developmental biologyOncologyDrug Resistance Neoplasm030220 oncology & carcinogenesisCancer cellMutationCancer researchbusinessRB1Tyrosine kinaseMicrotubule-Associated Proteinsnonsmokers
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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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Recent Advances in Desmoid Tumor Therapy

2020

The desmoid tumor is a locally aggressive proliferative disease within the family of soft-tissue sarcomas. Despite its relatively good prognosis, the clinical management of desmoid tumors requires constant multidisciplinary evaluation due to its highly variable clinical behavior. Recently, active surveillance has being regarded as the appropriate strategy at diagnosis, as indolent persistence or spontaneous regressions are not uncommon. Here, we review the most recent advances in desmoid tumor therapy, including low-dose chemotherapy and treatment with tyrosine kinase inhibitors. We also explore the recent improvements in our knowledge of the molecular biology of this disease, which are lea…

0301 basic medicineOncologyCancer Researchmedicine.medical_specialtymedicine.medical_treatmentProliferative diseasedesmoid tumorDiseaseReviewchemotherapylcsh:RC254-282aggressive fibromatosis03 medical and health sciences0302 clinical medicineInternal medicinedesmoid tumor; aggressive fibromatosis; active surveillance; chemotherapy; tyrosine kinase inhibitorstyrosine kinase inhibitorsmedicineChemotherapybusiness.industryactive surveillanceTumor therapyaggressive fibromatosimedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensClinical trialbody regions030104 developmental biologyOncology030220 oncology & carcinogenesisAggressive fibromatosisGood prognosisbusinessCancers
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Nintedanib in non-small cell lung cancer: from preclinical to approval

2015

Angiogenesis is a driving force of a tumor’s development. Targeting this process is an attractive option, as this is a feature shared by most of the solid tumors. A lot of antiangiogenic drugs have been developed following this path, including bevacizumab, sorafenib, sunitinib, vandetanib, ramucirumab, motesanib and many others. The latest drug of this class to be approved for patients with non-small cell lung cancer (NSCLC) was nintedanib, a triple angiokinase inhibitor. This molecule targets vascular endothelial growth factor (VEGF), platelet derived growth factor (PDGF) and fibroblast growth factor (FGF) pathways, avoiding the tumor’s switch to normal escape mechanisms. The pharmacokine…

Pulmonary and Respiratory MedicineSorafenibIndolesLung NeoplasmsBevacizumabBIBF1120Settore MED/06 - Oncologia Medicamedicine.drug_classDrug Evaluation PreclinicalAngiogenesis InhibitorsAntineoplastic AgentsAdenocarcinomaPharmacologyNSCLCVandetanibTyrosine-kinase inhibitorRamucirumabchemistry.chemical_compoundtyrosine kinase inhibitorCarcinoma Non-Small-Cell LungnintedanibmedicineMotesanibAnimalsHumansPharmacology (medical)Drug Approvalnon-small cell lung cancerlcsh:RC705-779Neovascularization PathologicSunitinibbusiness.industrylcsh:Diseases of the respiratory systemchemistryCancer researchNintedanibHuman medicinebusinessantiangiogenic drugmedicine.drugTherapeutic Advances in Respiratory Disease
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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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From molecular mechanisms to clinical management of antineoplastic drug-induced cardiovascular toxicity: A translational overview

2019

Significance: Antineoplastic therapies have significantly improved the prognosis of oncology patients. However, these treatments can bring to a higher incidence of side-effects, including the worrying cardiovascular toxicity (CTX). Recent Advances: Substantial evidence indicates multiple mechanisms of CTX, with redox mechanisms playing a key role. Recent data singled out mitochondria as key targets for antineoplastic drug-induced CTX; understanding the underlying mechanisms is, therefore, crucial for effective cardioprotection, without compromising the efficacy of anti-cancer treatments. Critical Issues: CTX can occur within a few days or many years after treatment. Type I CTX is associated…

Cardiovascular toxicityPhysiologymedicine.medical_treatmentAntineoplastic drugClinical BiochemistryAntineoplastic Agents030204 cardiovascular system & hematologyPharmacologyBiochemistryCardiac cellcancer immunotherapy; chemotherapy; ErbB2 inhibitors; oxidative/nitrosative stress; tyrosine kinase inhibitors; vascular endothelial growth factor; Antineoplastic Agents; Cardiotoxicity; Humans; Mitochondria; Oxidation-Reduction03 medical and health scienceschemistry.chemical_compoundErbB2 inhibitors cancer immunotherapy chemotherapy oxidative/nitrosative stress tyrosine kinase inhibitors vascular endothelial growth factor0302 clinical medicinetyrosine kinase inhibitorcancer immunotherapy; chemotherapy; ErbB2 inhibitors; oxidative/nitrosative stress; tyrosine kinase inhibitors; vascular endothelial growth factorChemotherapy; ErbB2 inhibitors; vascular endothelial growth factor; tyrosine kinase inhibitors; oxidative/nitrosative stress; cancer immunotherapyCancer immunotherapytyrosine kinase inhibitorsmedicineHumansChemotherapyMolecular BiologyGeneral Environmental ScienceCardioprotectionComprehensive Invited ReviewsChemotherapyErbB2 inhibitorcancer immunotherapyvascular endothelial growth factorbusiness.industryCell BiologyCardiotoxicityMitochondriaVascular endothelial growth factoroxidative/nitrosative streErbB2 inhibitorschemistry030220 oncology & carcinogenesisGeneral Earth and Planetary SciencesbusinessOxidation-ReductionAfter treatmentoxidative/nitrosative stress
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The Emerging Therapeutic Landscape of ALK Inhibitors in Non-Small Cell Lung Cancer.

2020

The treatment of metastatic non-small cell lung cancer (NSCLC) has undergone a paradigm shift over the last decade. Better molecular characterization of the disease has led to the rapid improvement of personalized medicine and the prompt delivery of targeted therapies to patients with NSCLC. The discovery of the EML4-ALK fusion gene in a limited subset of patients affected by NSCLC and the subsequent clinical development of crizotinib in 2011 has been an impressive milestone in lung cancer research. Unfortunately, acquired resistances regularly develop, hence disease progression occurs. Afterward, modern tyrosine kinase inhibitors (TKIs), such as ceritinib, alectinib, brigatinib, and lorlat…

0301 basic medicineOncologyAlectinibALK inhibitorsmedicine.medical_specialtybrigatinibBrigatinibmedicine.medical_treatmentPharmaceutical Sciencenon-small cell lung cancer (NSCLC)lcsh:Medicinelcsh:RS1-441ReviewALK inhibitorTargeted therapylcsh:Pharmacy and materia medica03 medical and health sciences0302 clinical medicinelorlatinibInternal medicineDrug DiscoveryMedicineAnaplastic lymphoma kinaseceritinibalectinibensartinibcrizotinibCrizotinibCeritinibbusiness.industrylcsh:Rmedicine.diseaseLorlatinibrespiratory tract diseasesnon-small cell lung cancer (NSCLC)030104 developmental biologytyrosine kinase inhibitors (TKIs)030220 oncology & carcinogenesisMolecular Medicinebusinessmedicine.drugPharmaceuticals (Basel, Switzerland)
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BCR-ABL1 Doubling-Times and Halving-Times May Predict CML Response to Tyrosine Kinase Inhibitors

2019

In Chronic Myeloid Leukemia (CML), successful treatment requires accurate molecular monitoring to evaluate disease response and provide timely interventions for patients failing to achieve the desired outcomes. We wanted to determine whether measuring BCR-ABL1 mRNA doubling-times (DTs) could distinguish inconsequential rises in the oncogene’s expression from resistance to tyrosine kinase inhibitors (TKIs). Thus, we retrospectively examined BCR-ABL1 evolution in 305 chronic-phase CML patients receiving imatinib mesylate (IM) as a first line treatment. Patients were subdivided in two groups: those with a confirmed rise in BCR-ABL1 transcripts without MR3.0 loss and those failing IM. We found …

0301 basic medicineOncologyCancer Researchmedicine.medical_specialtyDisease ResponseChronic Myeloid LeukemiaBCR-ABL1/ABL1IShalving-timelcsh:RC254-28203 medical and health sciences0302 clinical medicineInternal medicinehemic and lymphatic diseasesBCR-ABL1/ABL1; IS; Chronic Myeloid Leukemia; Doubling-time; Halving-time; Tyrosine kinase inhibitorstyrosine kinase inhibitorsmedicineDoubling timeOriginal ResearchBCR-ABL1/ABL1Oncogenebusiness.industryMyeloid leukemialcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensDiscontinuationdoubling-time030104 developmental biologyImatinib mesylateOncology030220 oncology & carcinogenesisCohortISBCR-ABL1/ABL1 ISbusinessTyrosine kinaseFrontiers in Oncology
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