Search results for "GFR"

showing 10 items of 206 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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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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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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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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Long Pentraxin 3-Mediated Fibroblast Growth Factor Trapping Impairs Fibrosarcoma Growth

2018

Fibrosarcomas are soft tissue mesenchymal tumors originating from transformed fibroblasts. Fibroblast growth factor-2 (FGF2) and its tyrosine-kinase receptors (FGFRs) play pivotal roles in fibrosarcoma onset and progression, FGF2 being actively produced by fibroblasts in all stages along their malignant transformation to the fibrosarcoma stage. The soluble pattern recognition receptor long pentraxin-3 (PTX3) is an extrinsic oncosuppressor whose expression is reduced in different tumor types, including soft tissue sarcomas, via hypermethylation of its gene promoter. PTX3 interacts with FGF2 and other FGF family members, thus acting as a multi-FGF antagonist able to inhibit FGF-dependent neov…

0301 basic medicineCancer ResearchFGF; FGF-trap; FGFR; fibrosarcoma; long pentraxin-3Fibroblast growth factorlcsh:RC254-282Malignant transformation03 medical and health sciences0302 clinical medicinemedicineFGFFibrosarcomaFibroblastReceptorneoplasmsOriginal ResearchFGF-trapintegumentary systemChemistryFGFRMesenchymal stem cellPTX3medicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens030104 developmental biologymedicine.anatomical_structurelong pentraxin-3OncologyFibroblast growth factor receptor030220 oncology & carcinogenesisCancer researchfibrosarcomaFrontiers in Oncology
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The PDGFRβ/ERK1/2 pathway regulates CDCP1 expression in triple-negative breast cancer

2018

Background CDCP1, a transmembrane protein with tumor pro-metastatic activity, was recently identified as a prognostic marker in TNBC, the most aggressive breast cancer subtype still lacking an effective molecular targeted therapy. The mechanisms driving CDCP1 over-expression are not fully understood, although several stimuli derived from tumor microenvironment, such as factors present in Wound Healing Fluids (WHFs), reportedly increase CDCP1 levels. Methods The expression of CDCP1, PDGFRβ and ERK1/2cell was tested by Western blot after stimulation of MDA-MB-231 cells with PDGF-BB and, similarly, in presence or not of ERK1/2 inhibitor in a panel of TNBC cell lines. Knock-down of PDGFRβ was e…

0301 basic medicineCancer ResearchMAP Kinase Signaling SystemCDCP1medicine.medical_treatmentPDGFRβPDGF-BBBecaplerminTriple Negative Breast NeoplasmsBiologylcsh:RC254-282Targeted therapyReceptor Platelet-Derived Growth Factor beta03 medical and health sciences0302 clinical medicineFISHDownregulation and upregulationWestern blotAntigens CDAntigens NeoplasmCell Line TumorGeneticsmedicineHumansRNA Small InterferingReceptorTriple-negative breast cancerMitogen-Activated Protein Kinase 1Tumor microenvironmentMitogen-Activated Protein Kinase 3ERK1/2medicine.diagnostic_testMiddle Agedlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensNeoplasm ProteinsUp-RegulationGene Expression Regulation Neoplastic030104 developmental biologyOncologyGene Knockdown Techniques030220 oncology & carcinogenesisCDCP1Cancer researchImmunohistochemistryFemaleCell Adhesion MoleculesTNBCResearch ArticleIHCBMC Cancer
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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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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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FGFR a promising druggable target in cancer: Molecular biology and new drugs.

2017

Abstract: Introduction: The Fibroblast Growth Factor Receptor (FGFR) family consists of Tyrosine Kinase Receptors (TKR) involved in several biological functions. Recently, alterations of FGFR have been reported to be important for progression and development of several cancers. In this setting, different studies are trying to evaluate the efficacy of different therapies targeting FGFR. Areas Covered: This review summarizes the current status of treatments targeting FGFR, focusing on the trials that are evaluating the FGFR profile as inclusion criteria: Multi-Target, Pan-FGFR Inhibitors and anti-FGF (Fibroblast Growth Factor)/FGFR Monoclonal Antibodies. Expert opinion: Most of the TKR share …

0301 basic medicineFibroblast Growth FactorDruggabilityFibroblast growth factorTyrosine-kinase inhibitorReceptor tyrosine kinase0302 clinical medicineNeoplasmsFGFR inhibitorsFGFMolecular Targeted TherapyCancerCancer; FGF; FGFR; FGFR inhibitors; Drug Resistance Neoplasm; Fibroblast Growth Factors; Gene Fusion; Humans; Molecular Targeted Therapy; Mutation; Neoplasms; Protein Kinase Inhibitors; Receptors Fibroblast Growth Factor; Signal Transduction; Hematology; Oncology; Geriatrics and GerontologybiologyFGFRHematologyFGFR inhibitorOncologyFibroblast growth factor receptor030220 oncology & carcinogenesisembryonic structuresSignal transductionbiological phenomena cell phenomena and immunityGene FusionHumanSignal Transductionmusculoskeletal diseasesanimal structuresmedicine.drug_classProtein Kinase Inhibitor03 medical and health sciencesmedicineHumansProtein Kinase InhibitorsCancer; FGF; FGFR; FGFR inhibitorsbusiness.industryCancermedicine.diseaseMolecular biologyReceptors Fibroblast Growth FactorFibroblast Growth Factors030104 developmental biologyDrug Resistance NeoplasmCancer cellMutationbiology.proteinNeoplasmHuman medicineGeriatrics and GerontologybusinessCritical reviews in oncology/hematology
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Amphiregulin contained in NSCLC-exosomes induces osteoclast differentiation through the activation of EGFR pathway

2017

AbstractNon-small cell lung cancer (NSCLC) remains the leading cause of cancer-related deaths worldwide. The majority of patients are diagnosed in advanced disease stage. Bone metastasis is the most frequent complication in NSCLC resulting in osteolytic lesions. The perfect balance between bone-resorbing osteoclasts and bone-forming osteoblasts activity is lost in bone metastasis, inducing osteoclastogenesis. In NSCLC, the epidermal growth factor receptor (EGFR) pathway is constitutively activated. EGFR binds Amphiregulin (AREG) that is overexpressed in several cancers such as colon, breast and lung. Its levels in plasma of NSCLC patients correlate with poor prognosis and AREG was recently …

0301 basic medicineLung NeoplasmsCellular differentiationAmphiregulin exosomes NSCLC EGFROsteoclastsExosomes NSCLC AmphiregulinNSCLCExosomesMice0302 clinical medicineSettore BIO/13 - Biologia ApplicataCarcinoma Non-Small-Cell LungMedicineEpidermal growth factor receptorRNA Small InterferingMultidisciplinarybiologyQProteolytic enzymesRBone metastasisCell Differentiation3. Good healthErbB ReceptorsGene Expression Regulation Neoplasticmedicine.anatomical_structureRANKL030220 oncology & carcinogenesisMedicineEngineering sciences. TechnologySciencePrimary Cell CultureBone NeoplasmsAmphiregulinArticle03 medical and health sciencesAmphiregulinOsteoclastCell Line TumorAnimalsHumansbusiness.industryRANK LigandBiological Transportmedicine.diseaseMicrovesiclesCoculture Techniquesrespiratory tract diseases030104 developmental biologyRAW 264.7 CellsImmunologybiology.proteinCancer researchbusiness
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