Search results for "epidermal growth factor"

showing 10 items of 227 documents

Analysis and comparison of autologous platelet-rich plasma preparation systems used in the treatment of enthesopathies: A preliminary study

2021

Background Autologous platelet-rich plasma (PRP) injection is an alternative but widely accepted method for the treatment of degenerative changes in tendon attachments known as enthesopathies. The PRP is considered a safe source for high concentrations of the growth factors involved in the healing process. Despite initial promising outcomes, many recent studies report conflicting results for this treatment. This may be due to differences in the concentrations of platelets and growth factors in PRPs obtained using different methods. Objectives The aim of this study was to compare PRP preparation systems in terms of morphotic components and selected growth factors to find the most appropriate…

Blood PlateletsMaleVascular Endothelial Growth Factor APlatelet-derived growth factormedicine.medical_treatmentPopulationMedicine (miscellaneous)EnthesopathyGeneral Biochemistry Genetics and Molecular Biologyplatelet-derived growth factorTransforming Growth Factor beta1AndrologyLeukocyte Countchemistry.chemical_compoundEpidermal growth factorgrowth factorsInternal MedicinemedicineHumansPharmacology (medical)PlateleteducationGenetics (clinical)Whole bloodeducation.field_of_studyEpidermal Growth FactorPlatelet-Rich Plasmabusiness.industryGrowth factorVascular endothelial growth factorchemistryPlatelet-rich plasmaReviews and References (medical)businessAdvances in Clinical and Experimental Medicine
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MS4A12 is a colon-selective store-operated calcium channel promoting malignant cell processes.

2008

AbstractUsing a data mining approach for the discovery of new targets for antibody therapy of colon cancer, we identified MS4A12, a sequence homologue of CD20. We show that MS4A12 is a cell surface protein. Expression analysis and immunohistochemistry revealed MS4A12 to be a colonic epithelial cell lineage gene confined to the apical membrane of colonocytes with strict transcriptional repression in all other normal tissue types. Expression is maintained upon malignant transformation in 63% of colon cancers. Ca2+ flux analyses disclosed that MS4A12 is a novel component of store-operated Ca2+ entry in intestinal cells. Using RNAi-mediated gene silencing, we show that loss of MS4A12 in LoVo co…

Calcium Channel Blockers/pharmacologyCancer ResearchColorectal cancerColonCalcium Channels/geneticsCell Differentiation/geneticsEpidermal Growth Factor/pharmacologyBiologyRNA Small Interfering/pharmacologyModels BiologicalMalignant transformationEpidermal growth factorCell Line TumormedicineMembrane Proteins/antagonists & inhibitorsHumansGrowth factor receptor inhibitorNeoplasm InvasivenessRNA Small InterferingEpidermal Growth FactorGene Expression ProfilingMembrane ProteinsColonic Neoplasms/geneticsCell DifferentiationApical membranemedicine.diseaseCalcium Channel BlockersColon/metabolismCell biologyChemokines/metabolismProtein Structure TertiaryGene Expression Regulation NeoplasticOncologyCell cultureOrgan SpecificityCancer cellColonic NeoplasmsDisease ProgressionCalcium ChannelsChemokinesA431 cellsCancer research
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Abstract LB-243: Cetuximab and Artesunate synergistically inhibit the invasion and distant metastasis of non-small cell lung cancer

2012

Abstract Cancer is a complex disease and multi step process evolving from malfunctions of molecules and their complex networks which regulate this process. The blockage of the cancer signalling network is crucial in the cancer treatment. In some cases, single drug therapy might not be comprehensive enough to inhibit the activity of secondary signals, feedback regulations and resistance to particular molecules, due to their abundant expression or activity. An understanding of these complex phenomena in cancer therapy for the benefit of patients is essential, especially since it bears the chance to establish novel concepts of combination drug therapy. In the present study, we have tried to fi…

Cancer ResearchCetuximabbiologybusiness.industryCell growthCancermedicine.diseasePrimary tumorMetastasisOncologyImmunologymedicineCancer researchbiology.proteinCytotoxic T cellEpidermal growth factor receptorLung cancerbusinessmedicine.drugCancer Research
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How to deal with second line dilemma in metastatic colorectal cancer? A systematic review and meta-analysis.

2019

e15006 Background: Monoclonal antibodies targeting epidermal growth factor receptor (EGFR) or vascular endothelial growth factor (VEGF) have demonstrated efficacy in combination with chemotherapy as second line for metastatic colorectal cancer (mCRC). However, there is still a paucity of evidence or guidelines suggesting the right sequential treatment in all RAS (KRAS/NRAS) wild type(wt)mCRC. Therefore, we aimed to evaluate the impact of these targeted therapies by reviewing literature data. Methods: We used Cochrane, EMBASE and Medline databases to select phase III clinical trials containing efficacy and safety data about chemotherapy (CT) or CT + targeted agents combination (Anti-VEGF an…

Cancer ResearchChemotherapybiologybusiness.industryColorectal cancermedicine.drug_classmedicine.medical_treatmentVEGF receptorsmedicine.diseaseMonoclonal antibodyVascular endothelial growth factorchemistry.chemical_compoundSecond lineOncologychemistryMeta-analysisCancer researchbiology.proteinMedicineEpidermal growth factor receptorbusinessJournal of Clinical Oncology
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Down-regulation of CYLD as a trigger for NF-κB activation and a mechanism of apoptotic resistance in hepatocellular carcinoma cells

2010

The cylindromatosis gene (CYLD) was identified as a tumor suppressor gene, which is mutated in familial cylindromatosis (Brooke-Spiegler syndrome), an autosomal-dominant predisposition to multiple tumors of the skin appendages. CYLD is a deubiquitinating enzyme acting as a negative regulator of the nuclear factor κB (NF-κB) signaling pathway by removing lysine-63-linked polyubiquitin chains from NF-κB activating proteins. In order to investigate the role of CYLD in apoptotic signaling in human hepatocellular carcinoma (HCC) cells, we first studied the expression levels of CYLD in HCC tissues. CYLD expression was lower in HCC both at protein and mRNA levels compared to the surrounding non-ma…

Cancer ResearchGene knockdownTumor suppressor geneOncogeneCell cycleBiologydigestive system diseasesDeubiquitinating Enzyme CYLDOncologyCancer researchbiology.proteinTumor necrosis factor alphaEpidermal growth factor receptorSignal transductionInternational Journal of Oncology
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β-Catenin Contributes to Lung Tumor Development Induced by EGFR Mutations

2014

Abstract The discovery of somatic mutations in EGFR and development of EGFR tyrosine kinase inhibitors (TKI) have revolutionized treatment for lung cancer. However, resistance to TKIs emerges in almost all patients and currently no effective treatment is available. Here, we show that β-catenin is essential for development of EGFR-mutated lung cancers. β-Catenin was upregulated and activated in EGFR-mutated cells. Mutant EGFR preferentially bound to and tyrosine phosphorylated β-catenin, leading to an increase in β-catenin–mediated transactivation, particularly in cells harboring the gefitinib/erlotinib-resistant gatekeeper EGFR-T790M mutation. Pharmacologic inhibition of β-catenin suppresse…

Cancer ResearchLung NeoplasmsCarcinogenesisAfatinibMutation MissenseAntineoplastic AgentsMice TransgenicAfatinibmedicine.disease_causeArticleTransactivationGefitinibCarcinoma Non-Small-Cell LungCell Line TumormedicineAnimalsHumansEpidermal growth factor receptorLung cancerbeta CateninMutationbiologyProtein Stabilitymedicine.diseaseXenograft Model Antitumor AssaysTumor BurdenUp-Regulationrespiratory tract diseasesErbB ReceptorsGene Expression Regulation NeoplasticHEK293 CellsOncologyDoxycyclineCateninImmunologyQuinazolinesCancer researchbiology.proteinCarcinogenesismedicine.drugCancer Research
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Temporal molecular and biological assessment of an erlotinib-resistant lung adenocarcinoma model reveals markers of tumor progression and treatment r…

2012

Abstract Patients with lung cancer with activating mutations in the EGF receptor (EGFR) kinase, who are treated long-term with tyrosine kinase inhibitors (TKI), often develop secondary mutations in EGFR associated with resistance. Mice engineered to develop lung adenocarcinomas driven by the human EGFR T790M resistance mutation are similarly resistant to the EGFR TKI erlotinib. By tumor volume endpoint analysis, these mouse tumors respond to BIBW 2992 (an irreversible EGFR/HER2 TKI) and rapamycin combination therapy. To correlate EGFR-driven changes in the lung with response to drug treatment, we conducted an integrative analysis of global transcriptome and metabolite profiling compared wit…

Cancer ResearchLung NeoplasmsCombination therapyAfatinibGene ExpressionAdenocarcinoma of LungCell Growth ProcessesAdenocarcinomaAfatinibArticleErlotinib HydrochlorideMiceAntineoplastic Combined Chemotherapy ProtocolsmedicineAnimalsEpidermal growth factor receptorLung cancerErlotinib HydrochlorideProtein Kinase InhibitorsSirolimusbiologymedicine.diseaserespiratory tract diseasesErbB ReceptorsOncologyTumor progressionDrug Resistance NeoplasmCancer researchbiology.proteinDisease ProgressionQuinazolinesErlotinibTyrosine kinasemedicine.drugTranscription FactorsCancer research
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Broad-spectrum Cross-resistance to Anticancer Drugs Mediated by Epidermal Growth Factor Receptor

2019

BACKGROUND The oncogenic role of epidermal growth factor receptor (EGFR) has been intensively studied. However, its emerging role in drug resistance has not been fully addressed. MATERIALS AND METHODS This study systematically investigated the correlation of mRNA and protein expression of EGFR, as well as gene amplification and mutations with the log-transformed half-maximal inhibitory concentration (log10IC50) values obtained from the NCI panel of 60 human tumor cell lines against 83 standard anticancer agents and the top 10 natural cytotoxic products previously screened by us. RESULTS EGFR protein expression, rather than other measurements, was most frequently associated with drug respons…

Cancer ResearchOncogenebiologyChemistryTopoisomeraseAntineoplastic AgentsGeneral MedicineDrug resistanceErbB Receptors03 medical and health sciences0302 clinical medicineOncologyDrug Resistance NeoplasmCell cultureCell Line TumorNeoplasms030220 oncology & carcinogenesisPharmacogenomicsbiology.proteinCancer researchHumansCytotoxic T cellRNA MessengerEpidermal growth factor receptorCross-resistanceAnticancer Research
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Co-expression of receptor tyrosine kinases in esophageal adenocarcinoma and squamous cell cancer.

2008

This study aimed to define the co-expression pattern of target receptor tyrosine kinases (RTKs) in human esophageal adenocarcinoma and squamous cell cancer. The co-expression pattern of vascular endothelial growth factor receptor (VEGFR)1-3, platelet-derived growth factor receptor (PDGFR)alpha/beta and epidermal growth factor receptor 1 (EGFR1) was analyzed by RT-PCR in 50 human esophageal cancers (35 adenocarcinomas and 15 squamous cell cancers). In addition, IHC staining was applied for the confirmation of the expression and analysis of RTK localisation. The adenocarcinoma samples revealed VEGFR1 (97%), VEGFR2 (94%), VEGFR3 (77%), PDGFRalpha (91%), PDGFRbeta (85%) and EGFR1 (97%) expressi…

Cancer ResearchPathologymedicine.medical_specialtyReceptor Platelet-Derived Growth Factor alphaEsophageal NeoplasmsAdenocarcinomaReceptor tyrosine kinaseReceptor Platelet-Derived Growth Factor betaGrowth factor receptormedicineHumansEpidermal growth factor receptorVascular Endothelial Growth Factor Receptor-1biologyOncogeneCancerReceptor Protein-Tyrosine KinasesGeneral Medicinemedicine.diseaseVascular Endothelial Growth Factor Receptor-3ImmunohistochemistryVascular Endothelial Growth Factor Receptor-2ErbB ReceptorsOncologyEpidermoid carcinomacardiovascular systembiology.proteinCancer researchCarcinoma Squamous CellAdenocarcinomaPlatelet-derived growth factor receptorOncology reports
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Mcl-1 is an anti-apoptotic factor for human hepatocellular carcinoma

2005

Defects in apoptosis signaling in hepatocytes contribute to tumorigenesis in hepatocellular carcinoma (HCC). In addition, treatment with chemotherapeutic drugs is often ineffective in HCC patients due to the apoptosis resistance of cancer cells. Anti-apoptotic members of the Bcl-2 family, including myeloid cell leukemia-1 (Mcl-1), which regulate intrinsic apoptosis induction at the mito-chondrial level, are often overexpressed in human cancer, and are implicated with disease grade and prognosis. Yet, little is known about the role of Mcl-1 in HCC. In this study, we analyzed the relevance of Mcl-1 expression for the apop-tosis resistance of human HCC. Mcl-1 protein expression was considerabl…

Cancer ResearchProgrammed cell deathCarcinoma HepatocellularApoptosisBiologyPhosphatidylinositol 3-KinasesEpidermal growth factorhemic and lymphatic diseasesTumor Cells CulturedmedicineHumansneoplasmsProtein kinase BPI3K/AKT/mTOR pathwayAkt/PKB signaling pathwayGene Expression ProfilingLiver NeoplasmsIntrinsic apoptosisPrognosisdigestive system diseasesNeoplasm ProteinsProto-Oncogene Proteins c-bcl-2OncologyImmunologyCancer cellCancer researchMyeloid Cell Leukemia Sequence 1 ProteinHepatocyte growth factorProto-Oncogene Proteins c-aktmedicine.drugInternational Journal of Oncology
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