Search results for "epiderma"

showing 10 items of 296 documents

Expression of angiogenic regulators, VEGF and leptin, is regulated by the EGF/PI3K/STAT3 pathway in colorectal cancer cells.

2009

Both leptin and vascular endothelial growth factor (VEGF) are growth and angiogenic cytokines that are upregulated in different types of cancer and have been implicated in neoplastic progression. Here we investigated the molecular mechanism by which leptin and VEGF expression are regulated in colon cancer by epidermal growth factor (EGF). In colon cancer cell line HT-29, EGF induced the binding of signal transducer and activator transcription 3 (STAT3) to STAT3 consensus motifs within the VEGF and leptin promoters and stimulated leptin and VEGF mRNA and protein synthesis. All these EGF effects were significantly blocked when HT-29 cells were treated with an inhibitor of the phosphoinositide…

LeptinSTAT3 Transcription FactorVascular Endothelial Growth Factor ASmall interfering RNAPhysiologyColorectal cancerClinical BiochemistryNeovascularization PhysiologicEGF/PI3K/STAT3colorectal cancerchemistry.chemical_compoundPhosphatidylinositol 3-KinasesEpidermal growth factormedicineHumansLY294002Gene SilencingRNA MessengerSTAT3Promoter Regions GeneticPI3K/AKT/mTOR pathwayCell NucleusbiologyEpidermal Growth FactorChemistryLeptinangiogenic regulators VEGF leptinCell Biologymedicine.diseaseUp-RegulationVascular endothelial growth factorGene Expression Regulation NeoplasticCancer researchbiology.proteinColorectal NeoplasmsHT29 Cellshormones hormone substitutes and hormone antagonistsProtein Binding
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Pro-invasive stimuli and the interacting protein Hsp70 favour the route of alpha-enolase to the cell surface

2017

AbstractCell surface expression of alpha-enolase, a glycolytic enzyme displaying moonlighting activities, has been shown to contribute to the motility and invasiveness of cancer cells through the protein non-enzymatic function of binding plasminogen and enhancing plasmin formation. Although a few recent records indicate the involvement of protein partners in the localization of alpha-enolase to the plasma membrane, the cellular mechanisms underlying surface exposure remain largely elusive. Searching for novel interactors and signalling pathways, we used low-metastatic breast cancer cells, a doxorubicin-resistant counterpart and a non-tumourigenic mammary epithelial cell line. Here, we demon…

Lipopolysaccharides0301 basic medicineAlpha-enolaseScienceCellPlasma protein bindingArticle03 medical and health sciencesCell MovementEpidermal growth factorCell Line TumormedicineHumansHSP70 Heat-Shock ProteinsRegulation of gene expressionMultidisciplinarybiologyQCell MembraneR3. Good healthCell biologyGene Expression Regulation NeoplasticSettore BIO/18 - Genetica030104 developmental biologymedicine.anatomical_structurePhosphopyruvate HydrataseChaperone (protein)Cancer cellbiology.proteinMedicineEnolase Hsp70 protein cell surface cancer biologyIntracellularProtein Binding
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FACIT collagen (1α-chain) is expressed by hemocytes and epidermis during the inflammatory response of the ascidian Ciona intestinalis

2007

Based on previous cloning and sequencing study, real-time PCR and in situ hybridization assays of the inflamed body wall of LPS-injected Ciona intestinalis showed the enhanced gene expression of a collagen with FACIT structural features (Ci-type IX-Col 1alpha-chain). By using specific antibodies raised against an opportunely chosen Ci-type IX-Col synthetic peptide, the fibroblast property of hemocytes challenged in vitro with LPS (at 4h) was displayed by flow cytometry, while immunocytochemistry identified hemocytes with large granules (morula cells) as collagen-producing cells. Hemocyte lysate supernatant analyzed in immunoblotting contained a 60 kDa band identifiable as 1alpha-chain-Ci-ty…

LipopolysaccharidesHemocytesImmunologyImmunocytochemistryIn situ hybridizationCollagen Type IXFACIT collagenExtracellular matrixParacrine CommunicationEscherichia colimedicineAnimalsCiona intestinalisFibroblastIn Situ HybridizationInflammationbiologyEpidermis (botany)Gene Expression Profilingbiology.organism_classificationImmunohistochemistryMolecular biologyCiona intestinalisExtracellular Matrixmedicine.anatomical_structureEpidermal CellsImmunologyEpidermisWound healingProtein Processing Post-TranslationalProcollagenDevelopmental BiologyDevelopmental & Comparative Immunology
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Compartmentalized production of CCL17 in vivo: strong inducibility in peripheral dendritic cells contrasts selective absence from the spleen.

2003

Dendritic cells (DCs)(*) fulfill an important regulatory function at the interface of the innate and adaptive immune system. The thymus and activation-regulated chemokine (TARC/CCL17) is produced by DCs and facilitates the attraction of activated T cells. Using a fluorescence-based in vivo reporter system, we show that CCL17 expression in mice is found in activated Langerhans cells and mature DCs located in various lymphoid and nonlymphoid organs, and is up-regulated after stimulation with Toll-like receptor ligands. DCs expressing CCL17 belong to the CD11b(+)CD8(-)Dec205(+) DC subset, including the myeloid-related DCs located in the subepithelial dome of Peyer's patches. CCL17-deficient mi…

LipopolysaccharidesLymphoid TissueGreen Fluorescent ProteinsDermatitis ContactArticleMicePhagocytosisGenes ReporterAnimalsListeriosisdendritic cellsCCL17/TARCcontact hypersensitivityMice Knockoutintegumentary systemGraft Survivaltransplant rejectionrespiratory systemCD11c AntigenToll-like receptorsMice Inbred C57BLLuminescent ProteinsEpidermal CellsChemokines CCLangerhans CellsGene TargetingHeart TransplantationChemokine CCL17EpidermisSpleenThe Journal of experimental medicine
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Multisciplinary management of patients with liver metastasis from colorectal cancer

2016

Abstract: Colorectal cancer (CRC) is one of the leading causes of cancer-related death. Surgery, radiotherapy and chemotherapy have been till now the main therapeutic strategies for disease control and improvement of the overall survival. Twenty-five per cent (25%) of CRC patients have clinically detectable liver metastases at the initial diagnosis and approximately 50% develop liver metastases during their disease course. Twenty-thirty per cent (20%-30%) are CRC patients with metastases confined to the liver. Some years ago various studies showed a curative potential for liver metastases resection. For this reason some authors proposed the conversion of unresectable liver metastases to res…

Liver metastase0301 basic medicinemedicine.medical_specialtyChemotherapy; Colorectal cancer; Liver metastases; Liver resection; Multidisciplinary team; Angiogenesis Inhibitors; Antineoplastic Combined Chemotherapy Protocols; Colorectal Neoplasms; Combined Modality Therapy; Disease Management; Hepatectomy; Humans; Liver Neoplasms; Receptor; Epidermal Growth Factor; GastroenterologyColorectal cancermedicine.medical_treatmentAngiogenesis InhibitorsColorectal NeoplasmReviewChemotherapy; Colorectal cancer; Liver metastases; Liver resection; Multidisciplinary team; Angiogenesis Inhibitors; Antineoplastic Combined Chemotherapy Protocols; Colorectal Neoplasms; Combined Modality Therapy; Disease Management; Hepatectomy; Humans; Liver Neoplasms; Receptor Epidermal Growth Factor; GastroenterologyMetastasis03 medical and health sciencesLiver metastases0302 clinical medicineAntineoplastic Combined Chemotherapy ProtocolsmedicineCombined Modality TherapyChemotherapyHepatectomyHumansDisease management (health)ChemotherapyAntineoplastic Combined Chemotherapy ProtocolLiver resectionEpidermal Growth Factorbusiness.industryGeneral surgeryHepatobiliary diseaseLiver NeoplasmsGastroenterologyDisease ManagementGeneral MedicineMultidisciplinary teammedicine.diseaseColorectal cancerCombined Modality TherapyRadiation therapyErbB Receptors030104 developmental biologyLiver Neoplasm030220 oncology & carcinogenesisReceptor Epidermal Growth FactorHuman medicineHepatectomybusinessColorectal NeoplasmsAngiogenesis InhibitorHumanReceptor
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Driver mutations and differential sensitivity to targeted therapies: a new approach to the treatment of lung adenocarcinoma

2010

The adenocarcinoma of the lung has recently shown peculiar molecular characteristics, which relate with both carcinogenesis and response to targeted drugs. Several molecular alterations have been defined as "driver mutations". These are responsible for both the initiation and maintenance of the malignancy. The epidermal growth factor receptor (EGFR) pathway is the main regulator of cell function and cancer development. It has a widely defined role in the occurrence of driver mutations. Up till now EGFR gene mutations, KRAS gene mutations and EML4-ALK fusion genes are the most widely recognized alterations involved in both the biology and the clinical management of lung adenocarcinoma. In th…

Lung NeoplasmsOncogene Proteins FusionSettore MED/06 - Oncologia MedicaEGFRGene ExpressionAdenocarcinomaGene mutationmedicine.disease_causeProto-Oncogene Proteins p21(ras)Phosphatidylinositol 3-KinasesPredictive Value of TestsProto-Oncogene ProteinsAntineoplastic Combined Chemotherapy ProtocolsmedicineAdenocarcinoma of the lungHumansRadiology Nuclear Medicine and imagingMolecular Targeted TherapyEpidermal growth factor receptorTyrosine kinase inhibitorsMutationbiologybusiness.industryDriver mutationGeneral MedicineProtein-Tyrosine KinasesPrognosismedicine.diseaseErbB ReceptorsTreatment OutcomeOncologyMutationImmunologyras ProteinsCancer researchbiology.proteinAdenocarcinomaKRASCarcinogenesisbusinessTyrosine kinaseAlgorithmsCancer Treatment Reviews
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Novel therapeutic strategies for patients with NSCLC that do not respond to treatment with EGFR inhibitors

2014

Abstract: Introduction: Treatment with epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) yields tumour responses in non-small cell lung cancer (NSCLC) patients harbouring activating EGFR mutations. However, even in long-lasting responses, resistance to EGFR TKIs invariably occurs. Areas covered: This review examines resistance mechanisms to EGFR TKI treatment, which mainly arise from secondary EGFR mutations. Other resistance-inducing processes include mesenchymal-epithelial transition factor (MET) amplification, epithelial-mesenchymal transformation, phenotypic change from NSCLC to small-cell lung carcinoma, and modifications in parallel signalling pathways. Current…

Lung NeoplasmsSettore MED/06 - Oncologia MedicaAfatinibNovel therapeutic strategiesLapatinibmedicine.disease_causeNSCLCT790Mchemistry.chemical_compoundErbB ReceptorsCarcinoma Non-Small-Cell LungAntineoplastic Combined Chemotherapy ProtocolsmedicineAnimalsHumansRadiology Nuclear Medicine and imagingEpidermal growth factor receptorProtein Kinase InhibitorsEGFR inhibitorsbiologybusiness.industryEGFR mutations; TKI inhibitors resistance; NSCLC; New drugs; Novel therapeutic strategiesGeneral MedicineNew drugEGFR mutationsCombined Modality TherapyDacomitinibrespiratory tract diseasesErbB ReceptorsNew drugsOncologychemistryDrug Resistance NeoplasmCancer researchbiology.proteinKRASHuman medicineEGFR mutationbusinessmedicine.drugTKI inhibitors resistanceCancer Treatment Reviews
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Activation of the PD-1 Pathway Contributes to Immune Escape in EGFR-Driven Lung Tumors

2013

Abstract The success in lung cancer therapy with programmed death (PD)-1 blockade suggests that immune escape mechanisms contribute to lung tumor pathogenesis. We identified a correlation between EGF receptor (EGFR) pathway activation and a signature of immunosuppression manifested by upregulation of PD-1, PD-L1, CTL antigen-4 (CTLA-4), and multiple tumor-promoting inflammatory cytokines. We observed decreased CTLs and increased markers of T-cell exhaustion in mouse models of EGFR-driven lung cancer. PD-1 antibody blockade improved the survival of mice with EGFR-driven adenocarcinomas by enhancing effector T-cell function and lowering the levels of tumor-promoting cytokines. Expression of m…

Lung NeoplasmsT-LymphocytesT cellProgrammed Cell Death 1 ReceptorMice TransgenicLymphocyte ActivationB7-H1 AntigenArticleCell LineProinflammatory cytokineMiceCarcinoma Non-Small-Cell LungTumor MicroenvironmentmedicineAnimalsHumansCytotoxic T cellEpidermal growth factor receptorLung cancerEGFR inhibitorsTumor microenvironmentbiologyOncogenesmedicine.diseaseErbB ReceptorsGene Expression Regulation NeoplasticMice Inbred C57BLmedicine.anatomical_structureOncologyTumor EscapeImmunologyCancer researchbiology.proteinCytokinesTumor EscapeSignal TransductionCancer Discovery
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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
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Use of intravenous immunoglobulins in Lyell syndrome: Experience of three cases

1996

We present our experience of treatment of the last three cases of Lyell syndrome we have observed. They are three female children, aged between 16 months and 3 years, who showed many features in common with severely burnt patients (large exuding lesions, severe reduction of circulating plasmatic volume, large denuded body surfaces, severe tendency to infections, ...). Therefore, together with the already known scheme of treatment (corticosteroids, correction of hydroelectrolitic balance, antimicrobials), we decided to use intravenous Immunoglobulins (IVIG), which had been already positively used in severely burnt patients. The favorable evolution of the affection in all three cases and the …

Lyell syndromeIntravenous Immunoglobulines (IVIG)Toxic Epidermal Necrolysis (TEN)
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