Search results for "TYROSINE KINASE"

showing 10 items of 362 documents

Prognostic significance of Focal Adhesion Kinase (FAK) in node-negative breast cancer.

2015

552 Background: Focal adhesion kinase (FAK) is a cytoplasmic tyrosine kinase playing an important role as a key mediator for signal transduction. We examined the subtype specific prognostic signifi...

CYTOPLASMIC TYROSINE KINASECancer ResearchPathologymedicine.medical_specialtybusiness.industrymedicine.diseaseNode negativeFocal adhesionMediatorBreast cancerOncologymedicineCancer researchSignal transductionbusinessJournal of Clinical Oncology
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Determination of essential biomarkers in lung cancer: a real-world data study in Spain with demographic, clinical, epidemiological and pathological c…

2022

Abstract Background The survival of patients with lung cancer has substantially increased in the last decade by about 15%. This increase is, basically, due to targeted therapies available for advanced stages and the emergence of immunotherapy itself. This work aims to study the situation of biomarker testing in Spain. Patients and methods The Thoracic Tumours Registry (TTR) is an observational, prospective, registry-based study that included patients diagnosed with lung cancer and other thoracic tumours, from September 2016 to 2020. This TTR study was sponsored by the Spanish Lung Cancer Group (GECP) Foundation, an independent, scientific, multidisciplinary oncology society that coordinates…

Cancer Research:Neoplasms::Neoplasms by Site::Thoracic Neoplasms::Respiratory Tract Neoplasms::Lung Neoplasms [DISEASES]Lung NeoplasmsTesting:Biological Factors::Biomarkers [CHEMICALS AND DRUGS]:factores biológicos::biomarcadores [COMPUESTOS QUÍMICOS Y DROGAS]Targeted therapiesPulmons - Càncer:neoplasias::neoplasias por localización::neoplasias torácicas::neoplasias del tracto respiratorio::neoplasias pulmonares [ENFERMEDADES]Carcinoma Non-Small-Cell LungProto-Oncogene ProteinsGeneticsBiomarkers TumorHumansProspective StudiesCàncerDemographyReceptor Protein-Tyrosine KinasesProtein-Tyrosine KinasesErbB ReceptorsOncologySpainPulmonsMarcadors bioquímicsBiomarkersMetastatic lung cancer
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STAT5 and STAT5 Inhibitors in Hematological Malignancies

2019

The JAK-STAT pathway is an important physiologic regulator of different cellular functions including proliferation, apoptosis, differentiation, and immunological responses. Out of six different STAT proteins, STAT5 plays its main role in hematopoiesis and constitutive STAT5 activation seems to be a key event in the pathogenesis of several hematological malignancies. This has led many researchers to develop compounds capable of inhibiting STAT5 activation or interfering with its functions. Several anti-STAT5 molecules have shown potent STAT5 inhibitory activity in vitro. However, compared to the large amount of clinical studies with JAK inhibitors that are currently widely used in the clini…

Cancer ResearchFLT3-ITDAntineoplastic Agents03 medical and health sciences0302 clinical medicineMyeloproliferative DisordersCancer stem cellSettore BIO/13 - Biologia Applicatahemic and lymphatic diseasesSTAT5 Transcription FactormedicineAnimalsHumansBCR-ABLSTAT5030304 developmental biologyPharmacology0303 health sciencesSTAT transcription factorbiologybusiness.industryfood and beveragesCancerHematopoietic stem cellMyeloid leukemiamedicine.diseaseSTAT5 inhibitorleukemia.Leukemiamedicine.anatomical_structureHematologic Neoplasms030220 oncology & carcinogenesisJak2V617Fbiology.proteinCancer researchSettore BIO/14 - FarmacologiaMolecular MedicinebusinessTyrosine kinase
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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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Temporal molecular and biological assessment of an erlotinib-resistant lung adenocarcinoma model reveals markers of tumor progression and treatment r…

2012

Abstract Patients with lung cancer with activating mutations in the EGF receptor (EGFR) kinase, who are treated long-term with tyrosine kinase inhibitors (TKI), often develop secondary mutations in EGFR associated with resistance. Mice engineered to develop lung adenocarcinomas driven by the human EGFR T790M resistance mutation are similarly resistant to the EGFR TKI erlotinib. By tumor volume endpoint analysis, these mouse tumors respond to BIBW 2992 (an irreversible EGFR/HER2 TKI) and rapamycin combination therapy. To correlate EGFR-driven changes in the lung with response to drug treatment, we conducted an integrative analysis of global transcriptome and metabolite profiling compared wit…

Cancer ResearchLung NeoplasmsCombination therapyAfatinibGene ExpressionAdenocarcinoma of LungCell Growth ProcessesAdenocarcinomaAfatinibArticleErlotinib HydrochlorideMiceAntineoplastic Combined Chemotherapy ProtocolsmedicineAnimalsEpidermal growth factor receptorLung cancerErlotinib HydrochlorideProtein Kinase InhibitorsSirolimusbiologymedicine.diseaserespiratory tract diseasesErbB ReceptorsOncologyTumor progressionDrug Resistance NeoplasmCancer researchbiology.proteinDisease ProgressionQuinazolinesErlotinibTyrosine kinasemedicine.drugTranscription FactorsCancer research
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Abstract B5: A BMP7 variant inhibits angiogenesis in vitro and in vivo in part by downregulating VEGFR2 and FGFR1 expression in endothelial cells.

2013

Abstract Glioblastoma multiforme (GBM), the most aggressive glioma, requires active angiogenesis for growth and survival. Bone morphogenetic proteins (BMPs), members of the TGF-β superfamily, have numerous biological activities including control of growth, differentiation, and vascular development. Previously, we demonstrated the use of a BMP7 variant (BMP7v) to differentiate glioblastoma stem-like cells (GSLCs) and significantly reduce their tumorigenic potential (Tate and Pallini et al. 2012). Using an in vitro co-culture endothelial cord formation assay, a surrogate of angiogenesis, and its cognate in vivo model, we investigated the role of BMP7v in VEGF, basic FGF (bFGF), tumor-driven a…

Cancer ResearchMatrigelbiologyAngiogenesisSMADFibroblast growth factorReceptor tyrosine kinaseEndothelial stem cellOncologyIn vivoMothers against decapentaplegic homolog 4Immunologybiology.proteinCancer researchMolecular Cancer Therapeutics
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Role of SHP2 for FLT3-dependent proliferation and transformation in 32D cells.

2008

Fms-like tyrosine kinase 3 (FLT3) is a class III receptor tyrosine kinase, which plays a role in proliferation and differentiation of B-cell progenitors, myelomonocytic and dendritic cells, as well as in the maintenance of pluripotent hematopoietic stem cells (reviewed in Stirewalt and Radich,1and Schmidt-Arras et al.2). Recently, FLT3 has received much attention as an important oncoprotein. Mutations in FLT3 that lead to constitutive activation are among the most common molecular lesions found in acute myeloid leukemia.3 The most prevalent type of mutations result in internal tandem duplications (ITD) of amino-acid stretches in the juxtamembrane domain of FLT3. FLT3-ITD is constitutively a…

Cancer ResearchMyeloidProtein Tyrosine Phosphatase Non-Receptor Type 11Biologymedicine.disease_causeReceptor tyrosine kinaseCell LineMicefluids and secretionshemic and lymphatic diseasesmedicineAnimalsHumansRNA Small InterferingCell ProliferationMice Inbred C3Hhemic and immune systemsHematologyHaematopoiesismedicine.anatomical_structureCell Transformation NeoplasticOncologyfms-Like Tyrosine Kinase 3Trk receptorembryonic structuresCancer researchbiology.proteinStem cellSignal transductionCarcinogenesisTyrosine kinaseSignal TransductionLeukemia
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Co-expression of receptor tyrosine kinases in esophageal adenocarcinoma and squamous cell cancer.

2008

This study aimed to define the co-expression pattern of target receptor tyrosine kinases (RTKs) in human esophageal adenocarcinoma and squamous cell cancer. The co-expression pattern of vascular endothelial growth factor receptor (VEGFR)1-3, platelet-derived growth factor receptor (PDGFR)alpha/beta and epidermal growth factor receptor 1 (EGFR1) was analyzed by RT-PCR in 50 human esophageal cancers (35 adenocarcinomas and 15 squamous cell cancers). In addition, IHC staining was applied for the confirmation of the expression and analysis of RTK localisation. The adenocarcinoma samples revealed VEGFR1 (97%), VEGFR2 (94%), VEGFR3 (77%), PDGFRalpha (91%), PDGFRbeta (85%) and EGFR1 (97%) expressi…

Cancer ResearchPathologymedicine.medical_specialtyReceptor Platelet-Derived Growth Factor alphaEsophageal NeoplasmsAdenocarcinomaReceptor tyrosine kinaseReceptor Platelet-Derived Growth Factor betaGrowth factor receptormedicineHumansEpidermal growth factor receptorVascular Endothelial Growth Factor Receptor-1biologyOncogeneCancerReceptor Protein-Tyrosine KinasesGeneral Medicinemedicine.diseaseVascular Endothelial Growth Factor Receptor-3ImmunohistochemistryVascular Endothelial Growth Factor Receptor-2ErbB ReceptorsOncologyEpidermoid carcinomacardiovascular systembiology.proteinCancer researchCarcinoma Squamous CellAdenocarcinomaPlatelet-derived growth factor receptorOncology reports
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A phase I study of MEHD7945A (MEHD), a first-in-class HER3/EGFR dual-action antibody, in patients (pts) with refractory/recurrent epithelial tumors: …

2012

2568 Background: Dysregulated human epidermal growth factor receptor tyrosine kinase (HER RTK) signaling is an important driver of tumor growth, metastasis, and survival. Extensive co-expression and heterodimerization suggest that simultaneous blockade of multiple HER RTKs may be more effective than blockade of a single RTK. MEHD is a novel dual-action human IgG1 antibody. Each antigen-binding fragment blocks ligand binding to HER3 or EGFR, and intended to inhibit signaling from all major ligand-dependent HER dimers. MEHD has single-agent activity in multiple tumor models including models resistant to anti-HER3 or anti-EGFR. Methods: This Phase I study evaluated safety, tolerability, pharm…

Cancer ResearchPathologymedicine.medical_specialtybiologybusiness.industrymedicine.diseaseReceptor tyrosine kinaseMetastasisBlockadeOncologyTolerabilityPharmacodynamicsCancer researchmedicinebiology.proteinImmunohistochemistryAntibodybusinessTyrosine kinaseJournal of Clinical Oncology
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