Search results for " tyrosine kinase inhibitors"

showing 10 items of 31 documents

Cardiotoxic Effects of Anti-VEGFR Tyrosine Kinase Inhibitors

2016

Angiogenesis is a key moment in tumor development and proliferation. Until recently oncologists did not know the mechanisms that were behind this phenomenon, but following the discoveries of Folkman and coworkers, they have gradually created and developed a series of drugs that act against angiogenesis by interacting with molecules belonging to the vascular endothelial growth factor (VEGFs) class and its receptors (VEGFRs) giving rise to anticancer effects. Tyrosine kinase inhibitors (TKIs) are a major class of these new anticancer agents, demonstrating high antitumor activity in a variety of "orphan" neoplasms (such as hepatocellular carcinoma, kidney cancer, sarcomas, etc.). The mechanism…

0301 basic medicineAngiogenesis; Cardio-oncology; Cardiotoxicity; Tyrosine kinase inhibitors; VEGF; VEGF pathway; Medicine (all)Settore MED/06 - Oncologia MedicaAngiogenesisTyrosine kinase inhibitorPharmacology03 medical and health scienceschemistry.chemical_compound0302 clinical medicineVEGF pathwaymedicineReceptorCardiotoxicitybusiness.industryMedicine (all)medicine.diseaseVEGFCardiotoxicityVascular endothelial growth factorAngiogenesiCardio-oncology030104 developmental biologyMechanism of actionchemistry030220 oncology & carcinogenesisHepatocellular carcinomamedicine.symptombusinessKidney cancerTyrosine kinase
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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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Targeting Angiogenesis in Biliary Tract Cancers: An Open Option

2017

Abstract: Biliary tract cancers (BTCs) are characterized by a bad prognosis and the armamentarium of drugs for their treatment is very poor. Although the inflammatory status of biliary tract represents the first step in the cancerogenesis, the microenvironment also plays a key role in the pathogenesis of BTCs, promoting tumor angiogenesis, invasion and metastasis. Several molecules, such as vascular endothelial growth factor (VEGF) and fibroblast growth factor (FGF), are involved in the angiogenesis process and their expression on tumor samples has been explored as prognostic marker in both cholangiocarcinoma and gallbladder cancer. Recent studies evaluated the genomic landscape of BTCs and…

0301 basic medicineMAPK/ERK pathwayVascular Endothelial Growth Factor AAngiogenesisDrug Evaluation PreclinicalTyrosine kinase inhibitorAngiogenesis InhibitorsReviewFibroblast growth factorCatalysiMetastasisAntineoplastic Agentlcsh:Chemistrychemistry.chemical_compoundangiogenesis0302 clinical medicinetyrosine kinase inhibitorsMolecular Targeted Therapylcsh:QH301-705.5SpectroscopyClinical Trials as TopicMonoclonal antibodieNeovascularization Pathologicvascular endothelial growth factorComputer Science Applications1707 Computer Vision and Pattern RecognitionGeneral MedicineComputer Science ApplicationsVascular endothelial growth factorGene Expression Regulation NeoplasticAngiogenesiChemistryBiliary Tract NeoplasmsTreatment OutcomeBiliary Tract Neoplasm030220 oncology & carcinogenesismonoclonal antibodiesTyrosine kinaseAngiogenesis InhibitorHumanSignal TransductionProtein Kinase InhibitorAntineoplastic Agentsbiliary tract cancersBiologyModels BiologicalAngiogenesis; Biliary tract cancers; Monoclonal antibodies; Tyrosine kinase inhibitors; Vascular endothelial growth factor; Angiogenesis Inhibitors; Animals; Antineoplastic Agents; Biliary Tract Neoplasms; Clinical Trials as Topic; Drug Evaluation Preclinical; Gene Expression Regulation Neoplastic; Genetic Variation; Humans; Models Biological; Neovascularization Pathologic; Protein Kinase Inhibitors; Signal Transduction; Treatment Outcome; Vascular Endothelial Growth Factor A; Molecular Targeted Therapy; Catalysis; Molecular Biology; Spectroscopy; Computer Science Applications1707 Computer Vision and Pattern Recognition; Physical and Theoretical Chemistry; Organic Chemistry; Inorganic ChemistryCatalysisInorganic Chemistry03 medical and health sciencesIn vivomedicineAnimalsHumansPhysical and Theoretical ChemistryGallbladder cancerMolecular BiologyProtein Kinase InhibitorsBiologyAnimalOrganic ChemistryGenetic Variationmedicine.disease030104 developmental biologychemistrylcsh:Biology (General)lcsh:QD1-999Immunologyangiogenesis; biliary tract cancers; monoclonal antibodies; tyrosine kinase inhibitors; vascular endothelial growth factorCancer researchBiliary tract cancerInternational Journal of Molecular Sciences
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Integrating Liquid Biopsy and Radiomics to Monitor Clonal Heterogeneity of EGFR-Positive Non-Small Cell Lung Cancer

2020

BackgroundEGFR-positive Non-small Cell Lung Cancer (NSCLC) is a dynamic entity and tumor progression and resistance to tyrosine kinase inhibitors (TKIs) arise from the accumulation, over time and across different disease sites, of subclonal genetic mutations. For instance, the occurrence of EGFR T790M is associated with resistance to gefitinib, erlotinib, and afatinib, while EGFR C797S causes osimertinib to lose activity. Sensitive technologies as radiomics and liquid biopsy have great potential to monitor tumor heterogeneity since they are both minimally invasive, easy to perform, and can be repeated over patient’s follow-up, enabling the extraction of valuable information. Yet, to date, t…

0301 basic medicineOncologyCancer Researchmedicine.medical_specialtyAfatinibEGFRprecision medicinelcsh:RC254-282cell free DNA; EGFR; liquid biopsy; non-small cell lung cancer; precision medicine; radiomics; tyrosine kinase inhibitors03 medical and health sciencesT790M0302 clinical medicineGefitinibInternal medicinetyrosine kinase inhibitorsmedicineOsimertinibLiquid biopsynon-small cell lung cancerOriginal ResearchReceiver operating characteristiccell free DNAliquid biopsybusiness.industrylcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens030104 developmental biologyOncologyTumor progressionradiomics030220 oncology & carcinogenesisErlotinibbusinessmedicine.drug
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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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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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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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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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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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