Search results for "EGF"

showing 10 items of 331 documents

Retinoic Acid affects Lung Adenocarcinoma growth by inducing differentiation via GATA6 activation and EGFR and Wnt inhibition

2016

AbstractA fundamental task in cancer research aims at the identification of new pharmacological therapies that can affect tumor growth. Differentiation therapy might exploit this function not only for hematological diseases, such as acute promyelocytic leukemia (APML) but also for epithelial tumors, including lung cancer. Here we show that Retinoic Acid (RA) arrests in vitro and in vivo the growth of Tyrosine Kinase Inhibitors (TKI) resistant Non Small Cell Lung Cancer (NSCLC). In particular, we found that RA induces G0/G1 cell cycle arrest in TKI resistant NSCLC cells and activates terminal differentiation programs by modulating the expression of GATA6, a key transcription factor involved …

0301 basic medicineAcute promyelocytic leukemiaScienceEGFRRetinoic acidMice NudeTretinoinBiologyArticle03 medical and health scienceschemistry.chemical_compoundDifferentiation therapySettore BIO/13 - Biologia ApplicataCarcinoma Non-Small-Cell LungCell Line TumorGATA6 Transcription FactormedicineRetinoic acidAnimalsHumansLung cancerProtein Kinase InhibitorsWnt Signaling PathwayTranscription factorCell ProliferationMultidisciplinaryQRWnt signaling pathwayCell Differentiationmedicine.diseaseG1 Phase Cell Cycle CheckpointsXenograft Model Antitumor Assaysrespiratory tract diseasesErbB Receptorslung cancerAnimals; Carcinoma Non-Small-Cell Lung; Cell Differentiation; Cell Line Tumor; Cell Proliferation; Drug Resistance Neoplasm; ErbB Receptors; G1 Phase Cell Cycle Checkpoints; GATA6 Transcription Factor; Humans; Mice Nude; Protein Kinase Inhibitors; Signal Transduction; Tretinoin; Wnt Signaling Pathway; Xenograft Model Antitumor Assays030104 developmental biologychemistryDrug Resistance NeoplasmImmunologyCancer researchMedicineAdenocarcinomaEngineering sciences. TechnologyTyrosine kinaseSignal Transduction
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Corrigendum: Resolvin D1 Modulates the Intracellular VEGF-Related miRNAs of Retinal Photoreceptors Challenged With High Glucose

2020

Abstract Stimulation of retinal photoreceptors with elevated glucose concentration (30 mM) for 96 hours, served as diabetic retinopathy in-vitro model to study Resolvin D1 (50 nM) effects on neovascularization. VEGF and anti-angiogenic miR-20a-3p, miR-20a-5p, miR-106a-5p and miR-20b expression was assessed either in photoreceptors exposed to HG or in exosomes released by those cells. High glucose increased VEGF levels and concurrently decreased anti-angiogenic miRNAs content in photoreceptors and exosomes. RvD1 reverted the effects of glucose damage in photoreceptors and exosomal pro-angiogenic potential, tested with the HUVEC angiogenesis assay. By activating FPR2 receptor, RvD1 modulated …

0301 basic medicineAngiogenesisStimulationexosomesretinal photoreceptors exosomes miRNAs resolvin D1 VEGFNeovascularization03 medical and health scienceschemistry.chemical_compoundretinal photoreceptors0302 clinical medicinemedicinePharmacology (medical)ReceptorOriginal ResearchPharmacologyChemistrylcsh:RM1-950CorrectionRetinalTransfectionVEGFMicrovesiclesCell biology030104 developmental biologylcsh:Therapeutics. Pharmacology030220 oncology & carcinogenesismiRNAsresolvin D1medicine.symptomIntracellularFrontiers in Pharmacology
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Expression Profile of VEGF-C, VEGF-D, and VEGFR-3 in Different Grades of Endometrial Cancer

2019

Background:Vascular endothelial growth factor (VEGF)-C, -D, and VEGF receptor-3 are proteins characterized as crucial for tumor lymphangiogenesis. It is accompanied by angiogenesis during wound healing, but also in the neoplastic process. The research studies have shown that the lymphatic system plays a key role in the progression of carcinogenesis.Objective:The aim of this study was to evaluate changes in the expression of VEGF-C, VEGF-D and VEGFR-3 in different grades of endometrial cancer (G1-G3).Methods:The study included 45 patients diagnosed with endometrial cancer (G1=17; G2=15; G3=13) and 15 patients without neoplastic changes. The expression of VEGF-C, VEGF-D, and VEGFR-3 was asses…

0301 basic medicineAngiogenesisVascular Endothelial Growth Factor CVascular Endothelial Growth Factor DVEGF-CPharmaceutical ScienceVEGF-Dmedicine.disease_causeMetastasisTranscriptome03 medical and health scienceschemistry.chemical_compound0302 clinical medicinemedicineHumansANOVANeovascularization Pathologicbusiness.industryEndometrial cancerCancerVascular Endothelial Growth Factor Receptor-3medicine.diseaseImmunohistochemistryEndometrial NeoplasmsLymphangiogenesisVEGFR-3lymphangiogenesisVascular endothelial growth factor030104 developmental biologychemistry030220 oncology & carcinogenesisendometrial cancerCancer researchFemaleNeoplasm GradingCarcinogenesisbusinessBiotechnologyCurrent Pharmaceutical Biotechnology
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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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Critical Roles of EGFR family members in breast cancer and breast cancer stem cells: Targets for therapy

2016

The roles of the epidermal growth factor receptor (EGFR) signaling pathway in various cancers including breast, bladder, brain, colorectal, esophageal, gastric, head and neck, hepatocellular, lung, neuroblastoma, ovarian, pancreatic, prostate, renal and other cancers have been keenly investigated since the 1980's. While the receptors and many downstream signaling molecules have been identified and characterized, there is still much to learn about this pathway and how its deregulation can lead to cancer and how it may be differentially regulated in various cell types. Multiple inhibitors to EGFR family members have been developed and many are in clinical use. Current research often focuses o…

0301 basic medicineCA15-3OncologyEGFR HER2 mIRs Cancer Stem Cells Drug Resistance Metastasismedicine.medical_specialtyEGFRDrug ResistancemIRCancer Stem CellBreast NeoplasmsNOMetastasisMetastasis03 medical and health sciences0302 clinical medicineBreast cancerCancer stem cellInternal medicineCancer Stem CellsHER2Drug DiscoverymicroRNAmedicineCancer Stem Cells; Drug Resistance; EGFR; HER2; Metastasis; mIRs; Pharmacology; Drug Discovery3003 Pharmaceutical ScienceAnimalsHumansEpidermal growth factor receptorPharmacologyCancer Stem Cells; Drug Resistance; EGFR; HER2; Metastasis; mIRsmIRsbiologybusiness.industryEGFR HER2 mIRs Cancer Stem Cells Drug Resistance Metastasis.Drug Discovery3003 Pharmaceutical ScienceCancermedicine.disease3. Good healthErbB Receptors030104 developmental biology030220 oncology & carcinogenesisbiology.proteinNeoplastic Stem CellsFemaleStem cellbusinessSignal Transduction
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Targeting prohibitins with chemical ligands inhibits KRAS-mediated lung tumours.

2017

KRAS is one of the most frequently mutated oncogenes in human non-small cell lung cancers (NSCLCs). RAS proteins trigger multiple effector signalling pathways including the highly conserved RAF-MAPK pathway. CRAF, a direct RAS effector protein, is required for KRAS-mediated tumourigenesis. Thus, the molecular mechanisms driving the activation of CRAF are intensively studied. Prohibitin 1 (PHB1) is an evolutionarily conserved adaptor protein and interaction of CRAF with PHB1 at the plasma membrane is essential for CRAF activation. Here, we demonstrate that PHB1 is highly expressed in NSCLC patients and correlates with poor survival. Targeting of PHB1 with two chemical ligands (rocaglamide an…

0301 basic medicineCancer ResearchEGF Family of ProteinsLung NeoplasmsBiologyLigandsProto-Oncogene Proteins p21(ras)03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineGrowth factor receptorRocaglamideEpidermal growth factorCarcinoma Non-Small-Cell LungCell Line TumorProhibitinsGeneticsAnimalsHumansMolecular Targeted TherapyProhibitinMolecular BiologyBenzofuransCell ProliferationRas InhibitorMice KnockoutTNF Receptor-Associated Factor 3EffectorXenograft Model Antitumor Assaysrespiratory tract diseasesCell biologyProto-Oncogene Proteins p21(ras)Gene Expression Regulation NeoplasticRepressor Proteins030104 developmental biologychemistry030220 oncology & carcinogenesisras Proteinsraf KinasesSignal transductionSignal TransductionOncogene
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PHD3 Controls Lung Cancer Metastasis and Resistance to EGFR Inhibitors through TGFα.

2018

Abstract Lung cancer is the leading cause of cancer-related death worldwide, in large part due to its high propensity to metastasize and to develop therapy resistance. Adaptive responses to hypoxia and epithelial–mesenchymal transition (EMT) are linked to tumor metastasis and drug resistance, but little is known about how oxygen sensing and EMT intersect to control these hallmarks of cancer. Here, we show that the oxygen sensor PHD3 links hypoxic signaling and EMT regulation in the lung tumor microenvironment. PHD3 was repressed by signals that induce EMT and acted as a negative regulator of EMT, metastasis, and therapeutic resistance. PHD3 depletion in tumors, which can be caused by the EM…

0301 basic medicineCancer ResearchEpithelial-Mesenchymal TransitionLung NeoplasmsMice NudeAntineoplastic AgentsSMADDrug resistanceMetastasisHypoxia-Inducible Factor-Proline DioxygenasesMitochondrial Proteins03 medical and health sciencesErlotinib HydrochlorideMice0302 clinical medicineDownregulation and upregulationCell Line TumorTumor MicroenvironmentMedicineAnimalsHumansNeoplasm MetastasisLung cancerProtein Kinase InhibitorsEGFR inhibitorsbusiness.industryIntracellular Signaling Peptides and ProteinsCancerTransforming Growth Factor alphamedicine.diseaseHCT116 CellsXenograft Model Antitumor AssaysCell HypoxiaErbB Receptors030104 developmental biologyOncologyA549 CellsDrug Resistance Neoplasm030220 oncology & carcinogenesisembryonic structuresCancer researchFemaleErlotinibbusinessApoptosis Regulatory Proteinsmedicine.drugCancer research
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Follow up analysis by exosomal miRNAs in EGFR mutated non-small cell lung cancer (NSCLC) patients during osimertinib (AZD9291) treatment: A potential…

2016

e23035Background: NSCLC patients harboring EGFR mutations are able to receive approved tyrosine kinase inhibitors (TKIs) but to better assess the treatment responses new tools are needed. Liquid bi...

0301 basic medicineCancer Researchbusiness.industrynon-small cell lung cancer (NSCLC)medicine.diseaserespiratory tract diseases03 medical and health sciences030104 developmental biology0302 clinical medicineOncologyEgfr mutation030220 oncology & carcinogenesismedicineCancer researchExosomal mirnasPrognostic biomarkerOsimertinibbusinessneoplasmsTyrosine kinaseJournal of Clinical Oncology
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EGFL7 - a potential therapeutic target for multiple sclerosis?

2018

0301 basic medicineEGF Family of ProteinsMultiple SclerosisClinical BiochemistryEndothelial Growth FactorsBlood–brain barrier03 medical and health sciences0302 clinical medicineDrug DiscoveryMedicineAnimalsHumansMolecular Targeted TherapyPharmacologybusiness.industryMultiple sclerosisNatalizumabCalcium-Binding Proteinsmedicine.disease030104 developmental biologymedicine.anatomical_structureBlood-Brain BarrierMolecular MedicineEGFL7businessNeuroscience030217 neurology & neurosurgeryExpert opinion on therapeutic targets
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Non-Small Cell Lung Cancer Harboring Concurrent EGFR Genomic Alterations: A Systematic Review and Critical Appraisal of the Double Dilemma

2021

The molecular pathways which promote lung cancer cell features have been broadly explored, leading to significant improvement in prognostic and diagnostic strategies. Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) have dramatically altered the treatment approach for patients with metastatic non-small cell lung cancer (NSCLC). Latest investigations by using next-generation sequencing (NGS) have shown that other oncogenic driver mutations, believed mutually exclusive for decades, could coexist in EGFR-mutated NSCLC patients. However, the exact clinical and pathological role of concomitant genomic aberrations needs to be investigated. In this systematic review, we ai…

0301 basic medicineEGFRNSCLC03 medical and health sciences0302 clinical medicinesystematic reviewPathologyRB1-214MedicineEpidermal growth factor receptorLung cancerPathologicalbiologybusiness.industrymedicine.diseaserespiratory tract diseasesconcurrent genomic alterationCritical appraisal030104 developmental biologyLung cancer cellconcurrent genomic alterationsNGS030220 oncology & carcinogenesisConcomitantCancer researchbiology.proteinNon small cellbusinessTyrosine kinase<i>EGFR</i>Journal of Molecular Pathology
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