Search results for " EGF"

showing 10 items of 48 documents

A Cre-inducible diphtheria toxin receptor mediates cell lineage ablation after toxin administration.

2004

A new system for lineage ablation is based on transgenic expression of a diphtheria toxin receptor (DTR) in mouse cells and application of diphtheria toxin (DT). To streamline this approach, we generated Cre-inducible DTR transgenic mice (iDTR) in which Cre-mediated excision of a STOP cassette renders cells sensitive to DT. We tested the iDTR strain by crossing to the T cell- and B cell-specific CD4-Cre and CD19-Cre strains, respectively, and observed efficient ablation of T and B cells after exposure to DT. In MOGi-Cre/iDTR double transgenic mice expressing Cre recombinase in oligodendrocytes, we observed myelin loss after intraperitoneal DT injections. Thus, DT crosses the blood-brain bar…

Genetically modified mouseCell SurvivalTransgeneT cellT-LymphocytesCellCre recombinaseApoptosisMice TransgenicReceptors Cell SurfaceBiologyBiochemistryCell LineMicemedicineAnimalsCell LineageDiphtheria ToxinReceptorMolecular BiologyDiphtheria toxinIntegrasesCell DifferentiationCell BiologyMolecular biologyRecombinant ProteinsOligodendrogliamedicine.anatomical_structureCell cultureIntercellular Signaling Peptides and ProteinsBiotechnologyHeparin-binding EGF-like Growth FactorNature methods
researchProduct

A novel in vivo inducible dendritic cell ablation model in mice

2010

Abstract Dendritic cells (DCs) are involved in T cell activation via their uptake and presentation of antigens. In vivo function of DCs was analyzed using transgenic mouse models that express diphtheria toxin receptor (DTR) or the diphtheria toxin-A subunit (DTA) under the control of the CD11c/Itgax promoter. However, CD11c+ cells are heterogeneous populations that contain several DC subsets. Thus, the in vivo function of each subset of DCs remains to be elucidated. Here, we describe a new inducible DC ablation model, in which DTR expression is induced under the CD11c/Itgax promoter after Cre-mediated excision of a stop cassette (CD11c-iDTR). Crossing of CD11c-iDTR mice with CAG-Cre transge…

Genetically modified mouseT cellBiophysicsCD11cCre recombinaseMice Transgenicchemical and pharmacologic phenomenaBiologyBiochemistryMiceAntigenIn vivomedicineAnimalsPromoter Regions GeneticMolecular BiologyIntegraseshemic and immune systemsDendritic CellsCell BiologyDendritic cellMolecular biologyIn vitroCD11c Antigenmedicine.anatomical_structureModels AnimalIntercellular Signaling Peptides and ProteinsHeparin-binding EGF-like Growth FactorBiochemical and Biophysical Research Communications
researchProduct

The role of cMET in non-small cell lung cancer resistant to EGFR-Inhibitors: Did we really find the target?

2014

Abstract: The advent of the epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) represented the most important innovation in NSCLC treatment over the last years. However, despite a great initial activity, secondary mutations in the same target, or different alterations in other molecular pathways, inevitably occur, leading to the emergence of acquired resistance, in median within the first year of treatment. In this scenario, the mesenchymal-epidermal transition (cMET) tyrosine kinase receptor and its natural ligand, the hepatocyte growth factor (HGF), seem to play an important role. Indeed either the overexpression or the amplification of cMET, as well as the overexpr…

Lung NeoplasmscMETcMET; cMET-Inhibitors; EGFR-TKIs resistance; HGF; NSCLC; Targeted therapies; Molecular Medicine; Pharmacology; Drug Discovery3003 Pharmaceutical Science; Clinical BiochemistryClinical BiochemistryAntineoplastic AgentsBiologyPharmacologyNSCLCReceptor tyrosine kinaseTargeted therapiesCarcinoma Non-Small-Cell LungDrug DiscoverymedicineHumansEpidermal growth factor receptorHGFLung cancerProtein Kinase InhibitorsEGFR inhibitorsEGFR-TKIs resistancePharmacologyClinical Trials as TopicPharmacology. TherapyDrug Discovery3003 Pharmaceutical ScienceAntibodies MonoclonalProto-Oncogene Proteins c-metmedicine.diseaseMolecular medicinerespiratory tract diseasesErbB ReceptorsDrug Resistance NeoplasmProto-Oncogene Proteins c-metbiology.proteinCancer researchMolecular MedicineDrug Therapy CombinationHepatocyte growth factorcMET-InhibitorTargeted therapiecMET-InhibitorsTyrosine kinasemedicine.drug
researchProduct

Roles of EGFR and KRAS and their downstream signaling pathways in pancreatic cancer and pancreatic cancer stem cells

2015

Pancreatic cancer is currently the fourth most common cancer, is increasing in incidence and soon will be the second leading cause of cancer death in the USA. This is a deadly malignancy with an incidence that approximates the mortality with 44,000 new cases and 36,000 deaths each year. Surgery, although only modestly successful, is the only curative option. However, due the locally aggressive nature and early metastasis, surgery can be performed on less than 20% of patients. Cytotoxic chemotherapy is palliative, has significant toxicity and improves survival very little. Thus new treatment paradigms are needed desperately. Due to the extremely high frequency of KRAS gene mutations (>90%) d…

MAPK/ERK pathwayCancer ResearchmiRsEGFRmedicine.disease_causeMetastasisProto-Oncogene Proteins p21(ras)Glycogen Synthase Kinase 3GeneticCancer stem cellKRaPancreatic cancerKRasGeneticsmedicineAnimalsHumansPTENEpidermal growth factor receptorMolecular BiologyPI3K/AKT/mTOR pathwayGSK-3biologyCancer stem cellsCancer stem cellmiRCancer stem cells; Drug resistance; EGFR; GSK-3; KRas; Metformin; miRsmedicine.diseaseMetforminErbB ReceptorsPancreatic NeoplasmsDrug resistanceNeoplastic Stem Cellsbiology.proteinCancer researchMolecular MedicineKRASSignal TransductionAdvances in Biological Regulation
researchProduct

The comparison of outcomes from tyrosine kinase inhibitor monotherapy in second- or third-line for advanced non-small-cell lung cancer patients with …

2016

// Giuseppe Bronte 1, * , Tindara Franchina 2, * , Massimiliano Alu 3, * , Giovanni Sortino 1 , Claudia Celesia 1 , Francesco Passiglia 1 , Giuseppina Savio 3 , Agata Laudani 3 , Alessandro Russo 2 , Antonio Picone 2 , Sergio Rizzo 1 , Michele De Tursi 4 , Elisabetta Gambale 4 , Viviana Bazan 1 , Clara Natoli 4 , Livio Blasi 3 , Vincenzo Adamo 2 , Antonio Russo 1 1 Department of Surgical, Oncological and Oral Sciences, University of Palermo, Palermo, Italy 2 Medical Oncology Unit-AOOR Papardo-Piemonte, Messina and Department of Human Pathology, University of Messina, Messina, Italy 3 Medical Oncology Unit, A.R.N.A.S. Civico, Palermo, Italy 4 Department of Medical, Oral and Biotechnological …

Male0301 basic medicineOncologymedicine.medical_specialtyLung Neoplasmsmedicine.drug_classEGFRTyrosine kinase inhibitorKaplan-Meier EstimateTyrosine-kinase inhibitorErlotinib Hydrochloride03 medical and health sciences0302 clinical medicineGefitinibCarcinoma Non-Small-Cell LungInternal medicinemedicineHumansChemotherapyErlotinib HydrochlorideLung cancerProtein Kinase InhibitorsChemotherapy EGFR Non-small-cell lung cancer Tyrosine kinase inhibitor OncologyAgedRetrospective StudiesAged 80 and overPerformance statusbusiness.industryChemotherapy; EGFR; Non-small-cell lung cancer; Tyrosine kinase inhibitor; OncologyGefitinibRetrospective cohort studyMiddle Agedmedicine.diseaserespiratory tract diseasesSurgeryErbB ReceptorsClinical trialTreatment Outcome030104 developmental biologyOncology030220 oncology & carcinogenesisMutationQuinazolinesFemaleErlotinibbusinessNon-small-cell lung cancerResearch Papermedicine.drug
researchProduct

Roles of signaling pathways in drug resistance, cancer initiating cells and cancer progression and metastasis

2014

The EGFR/PI3K/PTEN/Akt/mTORC pathway plays prominent roles in malignant transformation, prevention of apoptosis, drug resistance, cancer initiating cells (CICs) and metastasis. The expression of this pathway is frequently altered in breast and other cancers due to mutations at or aberrant expression of: HER2, EGFR1, PIK3CA, and PTEN as well as other oncogenes and tumor suppressor genes. miRs and epigenetic mechanisms of gene regulation are also important events which regulate this pathway. In some breast cancer cases, mutations at certain components of this pathway (e.g., PIK3CA) are associated with a better prognosis than breast cancers lacking these mutations. The expression of this pathw…

MaleOncologyCancer Researchmedicine.medical_treatmentTargeted therapyMetastasisTargeted therapyBreast cancerNeoplasmsNeoplasm MetastasisCancer stem cellsMedicine (all)Neoplasm ProteinsNeoplasm MetastasiGene Expression Regulation NeoplasticCell Transformation NeoplasticMolecular MedicineFemaleHormonal therapyHumanSignal Transductionmedicine.medical_specialtyEGFRBiologyNeoplasm ProteinBreast cancerGeneticCancer stem cellInternal medicineHER2GeneticsmedicineAnimalsHumansPTENMolecular BiologyProtein kinase BPI3K/AKT/mTOR pathwayCell ProliferationAnimalCancer stem cellTherapy resistanceCancermedicine.diseaseERDrug Resistance NeoplasmBreast cancer; Cancer stem cells; EGFR; ER; HER2; Hormonal therapy; Targeted therapy; Therapy resistancebiology.proteinCancer researchNeoplasm
researchProduct

The Adult Pituitary Shows Stem/Progenitor Cell Activation in Response to Injury and Is Capable of Regeneration

2012

The pituitary gland constitutes, together with the hypothalamus, the regulatory core of the endocrine system. Whether the gland is capable of cell regeneration after injury, in particular when suffered at adult age, is unknown. To investigate the adult pituitary's regenerative capacity and the response of its stem/progenitor cell compartment to damage, we constructed a transgenic mouse model to conditionally destroy pituitary cells. GHCre/iDTR mice express diphtheria toxin (DT) receptor after transcriptional activation by Cre recombinase, which is driven by the GH promoter. Treatment with DT for 3 d leads to gradual GH+ (somatotrope) cell obliteration with a final ablation grade of 80–90% 1…

Malemedicine.medical_specialtyPituitary glandTime FactorsSomatotropic cellMice TransgenicBiologyMiceEndocrinologySOX2Internal medicinemedicineAnimalsRegenerationCell LineageProgenitor cellPromoter Regions GeneticSOXB1 Transcription FactorsStem CellsDeoxyuridineEndothelial stem cellEndocrinologymedicine.anatomical_structureGrowth HormonePituitary GlandIntercellular Signaling Peptides and ProteinsFemaleStem cellHeparin-binding EGF-like Growth FactorAdult stem cellEndocrine glandEndocrinology
researchProduct

Regulatory T Cells and IL-10 Independently Counterregulate Cytotoxic T Lymphocyte Responses Induced by Transcutaneous Immunization

2011

Background: The imidazoquinoline derivate imiquimod induces inflammatory responses and protection against transplanted tumors when applied to the skin in combination with a cognate peptide epitope (transcutaneous immunization, TCI). Here we investigated the role of regulatory T cells (Treg) and the suppressive cytokine IL-10 in restricting TCI-induced cytotoxic T lymphocyte (CTL) responses. Methodology/Principal Findings: TCI was performed with an ointment containing the TLR7 agonist imiquimod and a CTL epitope was applied to the depilated back skin of C57BL/6 mice. Using specific antibodies and FoxP3-diphteria toxin receptor transgenic (DEREG) mice, we interrogated inhibiting factors after…

Mouselcsh:MedicineEpitopes T-LymphocyteAdaptive ImmunityT-Lymphocytes RegulatoryImmune toleranceMiceMedicineCytotoxic T celllcsh:ScienceImmune ResponseSkinMice KnockoutB-LymphocytesMultidisciplinaryImiquimodFOXP3hemic and immune systemsForkhead Transcription FactorsAnimal ModelsFlow CytometryInterleukin-10Interleukin 10medicine.anatomical_structureAminoquinolinesCytokinesIntercellular Signaling Peptides and ProteinsImmunotherapyResearch ArticleHeparin-binding EGF-like Growth FactorT cellImmune CellsImmunologychemical and pharmacologic phenomenaImmune SuppressionImmunomodulationImmune systemModel OrganismsImmune ToleranceAnimalsBiologyB cellbusiness.industrylcsh:RImmunityMice Inbred C57BLCTL*Immune SystemImmunologyImmunologic Techniqueslcsh:QImmunizationbusinessT-Lymphocytes CytotoxicPLoS ONE
researchProduct

Association of uric acid with kidney function and albuminuria: the Uric Acid Right for heArt Health (URRAH) Project

2021

Abstract Background Hyperuricemia is commonly observed in patients with chronic kidney disease (CKD). However, a better understanding of the relationship among uric acid (UA) values, glomerular filtration rate (GFR) and albuminuria may shed light on the mechanisms underlying the excess of cardiovascular mortality associated with both chronic kidney disease and hyperuricemia and lead to better risk stratification. Our main goal was to study the relationships between serum uric acid and kidney disease measures (namely estimated GFR [eGFR] and albuminuria) in a large cohort of individuals at cardiovascular risk from the URic acid Right for heArt Health (URRAH) Project database. Methods Clinica…

NephrologyAdultMalemedicine.medical_specialtySettore MED/09 - Medicina Interna030232 urology & nephrologyAllopurinolRenal functionHyperuricemia030204 cardiovascular system & hematologyKidneyurologic and male genital diseasesGastroenterology03 medical and health scienceschemistry.chemical_compound0302 clinical medicineSerum uric acidRisk FactorsInternal medicineDiabetes mellitusmedicineeGFRHumansAlbuminuriaHyperuricemiaRenal Insufficiency ChronicAgedbusiness.industryAlbuminuria; Cardiovascular risk; Serum uric acid; eGFRnutritional and metabolic diseaseseGFR.Middle Agedmedicine.diseaseCardiovascular riskUric AcidchemistryNephrologyAlbuminuriaUric acidAlbuminuria; Cardiovascular risk; eGFR; Serum uric acidOriginal ArticleFemalemedicine.symptombusinessmedicine.drugKidney diseaseGlomerular Filtration Rate
researchProduct

Quality of Life Analysis of TORCH, a Randomized Trial Testing First-Line Erlotinib Followed by Second-Line Cisplatin/Gemcitabine Chemotherapy in Adva…

2012

INTRODUCTION:: The TORCH (Tarceva or Chemotherapy) trial randomized patients with advanced non-small-cell lung cancer to first-line erlotinib followed by second-line cisplatin/gemcitabine versus. standard inverse sequence. The trial, designed to test noninferiority in overall survival, was stopped at interim analysis because of inferior survival in the experimental arm. Quality of life (QoL), a secondary outcome, is reported here. METHODS:: QoL was assessed at baseline and every 3 weeks during first-line, using European Organization for Research and Treatment of Cancer Quality of Life Questionnaire - Core 30 and QLQ-lung cancer specific module (LC13). Mean changes from baseline within arms …

OncologyMaleerlotinibLung NeoplasmsHealth-related quality of lifeNSCLCchemotherapyDeoxycytidinelaw.inventionRandomized controlled trialQuality of lifelawCarcinoma Non-Small-Cell LungSurveys and QuestionnairesAntineoplastic Combined Chemotherapy ProtocolsSurveys and QuestionnaireQuality of life analysis of TORCHErlotinib HydrochloridePrognosishumanitiesOncologyResearch DesignAdvanced non–small-cell lung cancerCarcinoma Squamous CellFemaleErlotinibRandomized trialmedicine.drugHumanPulmonary and Respiratory Medicinemedicine.medical_specialtyPrognosiEGFRFirst-line treatmentfirst-line erlotinibsecond-line cisplatin/gemcitabine chemotherapyAdenocarcinomaNOFollow-Up StudieErlotinib HydrochlorideInternal medicineadvanced non-small-cell lung cancermedicineHumansLung cancerAdvanced non-small-cell lung cancer; Chemotherapy; EGFR; Erlotinib; First-line treatment; Health-related quality of life; Randomized trialQuality of life analysis of TORCH first-line erlotinib second-line cisplatin/gemcitabine chemotherapy advanced non-small-cell lung cancer.AgedNeoplasm StagingSalvage TherapyAntineoplastic Combined Chemotherapy Protocolbusiness.industryQuestionnaireCancerQuinazolinemedicine.diseaseInterim analysisGemcitabineGemcitabineSurgeryLung Neoplasmquality of lifeQuinazolinesCarcinoma Large CellCisplatinNeoplasm Recurrence LocalbusinessFollow-Up Studies
researchProduct