Search results for "epiderma"

showing 10 items of 296 documents

New agents and approaches for targeting the RAS/RAF/MEK/ERK and PI3K/AKT/mTOR cell survival pathways.

2012

The Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR cascades are often activated by genetic alterations in upstream signaling molecules such as receptor tyrosine kinases (RTK). Targeting these pathways is often complex and can result in pathway activation depending on the presence of upstream mutations (e.g., Raf inhibitors induce Raf activation in cells with wild type (WT) RAF in the presence of mutant, activated RAS) and rapamycin can induce Akt activation. Targeting with inhibitors directed at two constituents of the same pathway or two different signaling pathways may be a more effective approach. This review will first evaluate potential uses of Raf, MEK, PI3K, Akt and mTOR inhibitors that have…

MAPK/ERK pathway0303 health sciencesCell signalingbiologyChemistryAKTApoptosisGrowth factorRafOncogens: Signaling pathway3. Good healthMalignant transformation03 medical and health sciences0302 clinical medicineApoptosis030220 oncology & carcinogenesisCancer researchbiology.proteinEpidermal growth factor receptorSignal transductionpi3kProtein kinase BRaPI3K/AKT/mTOR pathway030304 developmental biology
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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
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Signal transduction pathways of the epidermal growth factor receptor in colorectal cancer and their inhibition by small molecules.

2012

While prognostic factors can help to classify the standard risk of subpopulations of patients with the same tumor entity, it is still not possible to predict the response of individual patients to specific therapies. The reason for such wide variation in cancer therapy responses remains largely unknown. The field of chemotherapy is currently undergoing a paradigm shift from classical cytotoxic chemotherapy to targeted therapy in order to kill tumor cells more efficiently with fewer side effects on normal tissue. In the present review, we focus on colorectal carcinoma, which is one of the most frequent tumor types worldwide and represents a leading cause of cancer-related deaths. The signali…

MAPK/ERK pathwayColorectal cancerColonmedicine.medical_treatmentAntineoplastic AgentsBiochemistryTargeted therapySmall Molecule LibrariesGrowth factor receptorDrug DiscoverymedicinePTENAnimalsHumansGrowth factor receptor inhibitorEpidermal growth factor receptorMolecular Targeted TherapyPI3K/AKT/mTOR pathwayPharmacologybiologybusiness.industryOrganic ChemistryRectummedicine.diseaseErbB ReceptorsDrug Resistance NeoplasmCancer researchbiology.proteinMolecular MedicinebusinessColorectal NeoplasmsSignal TransductionCurrent medicinal chemistry
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Ability of nanocrystalline hydroxyapatite paste to promote human periodontal ligament cell proliferation.

2008

Recent studies indicate that nanocrystalline hydroxyapatite (nano-HA) paste represents a promising class of bone graft substitute. However, the underlying molecular mechanisms of nano-HA function have not yet been determined. This study was conducted to investigate the proliferation of human periodontal ligament (PDL) cells cultured in the presence of nano-HA paste and to characterize associated changes in intracellular signaling pathways. Cultured PDL cells were stimulated with nano-HA paste and enamel matrix derivative (EMD) in a soluble form. Proliferation of PDL cells was determined by incorporation of bromodeoxyuridine (BrdU) in the DNA of proliferating cells. In order to understand th…

MAPK/ERK pathwayPeriodontal LigamentBlotting Westernchemistry.chemical_compoundDental Enamel ProteinsPeriodontal fiberHumansRegenerationEpidermal growth factor receptorPhosphorylationGeneral DentistryProtein kinase BCells CulturedCell ProliferationMitogen-Activated Protein Kinase 1biologyChemistryCell growthKinaseAnatomyFibroblastsCell biologyErbB ReceptorsDurapatiteBone Substitutesbiology.proteinPhosphorylationNanoparticlesProto-Oncogene Proteins c-aktBromodeoxyuridineJournal of oral science
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Pathological significance and prognostic value of surfactant protein D in cancer

2018

Surfactant protein D (SP-D) is a pattern recognition molecule belonging to the Collectin (collagen-containing C-type lectin) family that has pulmonary as well as extra-pulmonary existence. In the lungs, it is a well-established opsonin that can agglutinate a range of microbes, and enhance their clearance via phagocytosis and super-oxidative burst. It can interfere with allergen–IgE interaction and suppress basophil and mast cell activation. However, it is now becoming evident that SP-D is likely to be an innate immune surveillance molecule against tumor development. SP-D has been shown to induce apoptosis in sensitized eosinophils derived from allergic patients and a leukemic cell line via …

Male0301 basic medicineLung NeoplasmsDatasets as Topic0302 clinical medicineEpidermal growth factorNeoplasmsImmunology and AllergyRNA NeoplasmOriginal ResearchCancerOvarian NeoplasmsInnate immunitySurfactant protein DBioinformatics analysiPrognosisPulmonary Surfactant-Associated Protein DImmunohistochemistryTumor microenvironment030220 oncology & carcinogenesisAdenocarcinomaFemaleCancersBreast NeoplasmHumanlcsh:Immunologic diseases. AllergyPrognosiImmunologyBreast NeoplasmsBiology03 medical and health sciencesImmune systemBioinformatics analysisStomach NeoplasmsStomach NeoplasmBiomarkers TumormedicineHumansComputer SimulationLung cancerTumor microenvironmentOvarian NeoplasmComputational BiologySurfactant protein DCancermedicine.diseaseSurvival AnalysisLung NeoplasmImmune surveillance030104 developmental biologyCancer researchNeoplasmBioinformatics analysis; Cancers; Immune surveillance; Immunohistochemistry; Innate immunity; Surfactant protein D; Tumor microenvironment; Immunology and Allergy; Immunologylcsh:RC581-607Ovarian cancer
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Additive effects of cherlerythrine chloride combination with erlotinib in human non-small cell lung cancer cells

2017

Several studies implicate that lung cancer progression is governed by the interaction between epidermal growth factor receptor (EGFR) signaling and protein kinase C (PKC) pathways. Combined the targeting of EGFR and PKC may have an additive or synergistic effects in lung cancer treatment. The aim of this study is to explore the potential utility by inhibiting these two pathways with the combination of erlotinib and chelerythrine chloride in non-small cell lung cancer (NSCLC) cell lines. The erlotinib-less sensitive cell lines SK-MES-1 and A549 were treated with erlotinib or chelerythrine by themselves or in combination with each other. The cell viability, clonogenic survival, cell migration…

Male0301 basic medicineOncologyCell signalingLung NeoplasmsCancer Treatmentlcsh:MedicineApoptosisMice SCIDSignal transductionLung and Intrathoracic TumorsMicechemistry.chemical_compoundMice Inbred NODCarcinoma Non-Small-Cell LungMedicine and Health SciencesEpidermal growth factor receptorPhosphorylationlcsh:ScienceErlotinib HydrochlorideMultidisciplinaryCell DeathbiologyPharmaceuticsChemistrySignaling cascadesFlow CytometryErbB ReceptorsCell MotilityOncologyCell ProcessesDrug Therapy CombinationErlotinibSignal transductionEGFR signalingResearch Articlemedicine.drugmedicine.medical_specialtyMAPK signaling cascadesCell MigrationErlotinib Hydrochloride03 medical and health sciencesDrug TherapyCell Line TumorInternal medicinemedicineAnimalsHumansViability assayLung cancerBenzophenanthridineslcsh:RCancers and NeoplasmsBiology and Life SciencesCell Biologymedicine.diseaseXenograft Model Antitumor AssaysNon-Small Cell Lung Cancerrespiratory tract diseases030104 developmental biologyChelerythrineApoptosisCancer researchbiology.proteinlcsh:QDevelopmental BiologyPLOS ONE
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A Phase Ib Dose-Escalation Study of the Safety, Tolerability, and Pharmacokinetics of Cobimetinib and Duligotuzumab in Patients with Previously Treat…

2017

Abstract Lessons Learned Cobimetinib and duligotuzumab were well tolerated as single agents and in combination with other agents. The cobimetinib and duligotuzumab combination was associated with increased toxicity, most notably gastrointestinal, and limited efficacy in the patient population tested. Background KRAS-mutant tumors possess abnormal mitogen-activated protein kinases (MAPK) pathway signaling, leading to dysregulated cell proliferation. Cobimetinib blocks MAPK signaling. The dual-action antibody duligotuzumab (MEHD7945A) inhibits ligand binding to both epidermal growth factor receptor (EGFR) and human epidermal growth factor receptor 3 (HER3). Blockade of EGFR/HER3 and inhibitio…

Male0301 basic medicineOncologyMAPK/ERK pathwayCancer ResearchReceptor ErbB-3MAP Kinase Kinase 1Administration Oralmedicine.disease_causechemistry.chemical_compound0302 clinical medicinePiperidinesAntineoplastic Combined Chemotherapy ProtocolsMedicineProspective StudiesEpidermal growth factor receptor31biologyMiddle AgedErbB ReceptorsTreatment OutcomeOncologyTolerability030220 oncology & carcinogenesisFemaleDrug EruptionsKRASmedicine.symptomColorectal NeoplasmsSignal TransductionAdultmedicine.medical_specialty4HypokalemiaAcneiform eruptionProto-Oncogene Proteins p21(ras)03 medical and health sciencesAcneiform EruptionsInternal medicineHumansAdverse effectAgedNeoplasm StagingCobimetinibDose-Response Relationship Drugbusiness.industryClinical Trial Resultsmedicine.disease030104 developmental biologychemistryAstheniaImmunoglobulin Gbiology.proteinAzetidinesbusinessProgressive diseaseThe Oncologist
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Adaptive physiological water conservation explains hypertension and muscle catabolism in experimental chronic renal failure

2021

Abstract Aim We have reported earlier that a high salt intake triggered an aestivation‐like natriuretic‐ureotelic body water conservation response that lowered muscle mass and increased blood pressure. Here, we tested the hypothesis that a similar adaptive water conservation response occurs in experimental chronic renal failure. Methods In four subsequent experiments in Sprague Dawley rats, we used surgical 5/6 renal mass reduction (5/6 Nx) to induce chronic renal failure. We studied solute and water excretion in 24‐hour metabolic cage experiments, chronic blood pressure by radiotelemetry, chronic metabolic adjustment in liver and skeletal muscle by metabolomics and selected enzyme activity…

Male0301 basic medicinePhysiologyBody waterBlood Pressure030204 cardiovascular system & hematologyRats Sprague-Dawley0302 clinical medicineRegular Paperdouble‐barrier conceptmuscle mass losstransaminationKidneyglycine methylationMusclesurine concentrationglucose‐alanine‐shuttlepurine metabolismaestivationmedicine.anatomical_structuremedicine.drugbody watermedicine.medical_specialtykidneyskinhypertensionorganic osmolytesliverCardivascular PhysiologyNorepinephrine (medication)03 medical and health sciencesCopeptinhepato‐renalInternal medicinemedicineurea cycleAnimalsHumansbody sodiumSalt intakeMuscle SkeletalTransepidermal water lossConservation of Water Resourcesbusiness.industrySkeletal muscletransepidermal water lossWaterdehydrationRats030104 developmental biologyBlood pressureEndocrinologyCardiovascular and Metabolic DiseasesKidney Failure ChronicbusinessActa Physiologica (Oxford, England)
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EGFR gene copy number decreases during anti-EGFR antibody therapy in colorectal cancer

2018

Epidermal growth factor receptor (EGFR) gene copy number (GCN) increase is associated with a favorable anti-EGFR antibody treatment response in RAS wild-type metastatic colorectal cancer. However, there are limited and comparative data regarding the EGFR GCN in primary colorectal cancer tumors and corresponding metastases or the effect of anti-EGFR antibody treatment on EGFR GCN in recurrent disease. In addition, little is known about the potential EGFR GCN changes during anti-EGFR therapy in comparison with other treatment regimens. EGFR GCN was analyzed by EGFR immunohistochemistry-guided silver in situ hybridization in primary and corresponding recurrent local or metastatic tumors from 8…

Male0301 basic medicineTime FactorsColorectal cancerBLOCKADEGene DosageCetuximabmedicine.disease_causeAntineoplastic Agents Immunological0302 clinical medicinePREDICTS RESPONSEMedicineHETEROGENEITYBENEFITCopy-number variationEpidermal growth factor receptorIn Situ Hybridization FluorescenceAged 80 and overbiologyPanitumumabvasta-aineetMiddle AgedImmunohistochemistry3. Good healthErbB ReceptorsGene Expression Regulation NeoplasticTreatment OutcomeRAS MUTATIONSChemotherapy Adjuvant030220 oncology & carcinogenesisFemaleKRASAntibodyColorectal NeoplasmsAdultgene copy numbermedicine.drug_classCETUXIMAB THERAPY3122 Cancerssilver in situ hybridizationDown-Regulationcolorectal cancerIn situ hybridizationAdenocarcinomaMonoclonal antibodyta3111Pathology and Forensic MedicineProto-Oncogene Proteins p21(ras)03 medical and health sciencesKRASHumansWILD-TYPEMETAANALYSISAgedRetrospective Studiessyöpähoidotbusiness.industrymedicine.diseaseta3122Blockadeperäsuolisyöpä030104 developmental biologymonoclonal antibodyMutationCancer researchbiology.protein3111 BiomedicineNeoplasm Recurrence Localbusinessepidermal growth factor receptorACQUIRED-RESISTANCEHuman Pathology
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Metformin induces an agonist-specific increase in albumin production by primary cultured rat hepatocytes

1995

Abstract Metformin (MET) is known to increase several biological effects of insulin (INS), but there is no information concerning its direct effects on protein synthesis. We studied the action of MET on albumin production by primary cultures of freshly isolated rat hepatocytes, alone or in combination with various agonists: INS, IGF-1, EGF, thyroxin, and dexamethasone. While having no effect alone, MET in vitro potentiates the effects of INS, IGF-1, and EGF. When this increasing effect toward INS was studied over a broad concentration range, MET appeared to improve low-acting INS levels and to intensify the maximal INS effects. In contrast, MET did not change the production of albumin stimu…

MaleAgonistmedicine.medical_specialtyTime FactorsCell Survivalmedicine.drug_classBiologyBiochemistryIn vivoCell surface receptorAlbuminsInternal medicinemedicineAnimalsInsulinInsulin-Like Growth Factor IRats WistarCells CulturedPharmacologyEpidermal Growth FactorBody WeightAlbuminMetforminIn vitroRatsMetforminmedicine.anatomical_structureEndocrinologyLiverCell cultureHepatocytemedicine.drugBiochemical Pharmacology
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