Search results for "eGFR"

showing 10 items of 150 documents

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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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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Safety and efficacy of afatinib as add-on to standard therapy of gemcitabine/cisplatin in chemotherapy-naive patients with advanced biliary tract can…

2019

Background To date, the cornerstone of treatment in patients with advanced or metastatic cholangiocarcinoma (CCA) is systemic chemotherapy based on a combination of gemcitabine and a platinum derivative. Other therapeutic approaches including targeted agents and tyrosine kinase inhibitors (TKI) have demonstrated disappointing results, highlighting the complexity of CCA. Recently, drugs aiming at the inhibition of HER-receptors have shown first therapeutic benefit in patients with late stage disease. The aim of this phase I study was to test the dose level toxicities (DLTs), safety and efficacy of afatinib, a highly specific panErbB family receptor TKI, in chemotherapy naive patients with ad…

Male0301 basic medicineOncologyCancer ResearchAfatinibDeoxycytidineTranslational Research BiomedicalCholangiocarcinoma0302 clinical medicineSurgical oncologyAntineoplastic Combined Chemotherapy ProtocolsNeoplasm Metastasismedia_commonAged 80 and overpanHER inhibitionMiddle Agedlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensImmunohistochemistryErbB ReceptorsBiliary Tract NeoplasmsTreatment OutcomeOncology030220 oncology & carcinogenesisBiomarker (medicine)FemaleTyrosine kinaseSignal TransductionResearch Articlemedicine.drugAdultDrugmedicine.medical_specialtyBIBW 2992media_common.quotation_subjectEGFRAfatiniblcsh:RC254-28203 medical and health sciencesInternal medicineGeneticsmedicineHumansProgression-free survivalAgedNeoplasm StagingCisplatinbusiness.industryGemcitabineGemcitabine030104 developmental biologyCisplatinbusinessBiomarkersBMC 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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Prognostic and predictive value of primary tumour side in patients with RAS wild-type metastatic colorectal cancer treated with chemotherapy and EGFR…

2017

BACKGROUND: There is increasing evidence that metastatic colorectal cancer (mCRC) is a genetically heterogeneous disease and that tumours arising from different sides of the colon (left versus right) have different clinical outcomes. Furthermore, previous analyses comparing the activity of different classes of targeted agents in patients with KRAS wild-type (wt) or RAS wt mCRC suggest that primary tumour location (side), might be both prognostic and predictive for clinical outcome. METHODS: This retrospective analysis investigated the prognostic and predictive influence of the localization of the primary tumour in patients with unresectable RAS wt mCRC included in six randomized trials (CRY…

Male0301 basic medicineOncologyColorectal cancermedicine.medical_treatmentCetuximabmedicine.disease_causeEGFR Antibody0302 clinical medicineAntineoplastic Agents ImmunologicalNeoplasias ColorrectaisMedicineNeoplasm MetastasisRandomized Controlled Trials as Topicpredictive valuePanitumumabHazard ratiotumour sideAntibodies MonoclonalHematologyPrognosisChemotherapy regimenErbB ReceptorsBevacizumabTreatment OutcomeOncology030220 oncology & carcinogenesisFemaleKRASColorectal Neoplasmsmedicine.drugmedicine.medical_specialtyBevacizumabcolorectal cancerGenes ras03 medical and health sciencesAnticorpos MonoclonaisInternal medicineHumansChemotherapybusiness.industryAntineoplásicos ImunológicosOdds ratiomedicine.diseaserandomised trial030104 developmental biologyGenes rasHuman medicinebusinessprognosticanti-EGFR treatment
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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
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Erratum to: Cetuximab-induced skin exanthema: prophylactic and reactive skin therapy are equally effective

2013

Purpose Treatment with cetuximab is accompanied by the development of an acneiform follicular skin exanthema in more than 80 % of patients. Severe exanthema (grade III/IV) develops in about 9–19 % of patients with the necessity of cetuximab dose reduction or cessation. Methods The study presented was a retrospective analysis of 50 gastrointestinal cancer patients treated with cetuximab in combination with either FOLFIRI or FOLFOX. One cohort of 15 patients received an in-house reactive skin protocol upon development of an exanthema. A second cohort of 15 patients received a skin prophylaxis starting with the first dose of cetuximab before clinical signs of toxicity. A third historic group o…

MaleCancer ResearchColorectal cancerAdministration TopicalAdministration OralCetuximabMinocyclineGastroenterologyPeritoneal NeoplasmPeritoneal NeoplasmsGastrointestinal NeoplasmsSkinHematologyintegumentary systemCetuximabTherapy reactiveMultimodal therapyVitamin K 1General MedicineMiddle AgedCombined Modality TherapyAnti-Bacterial AgentsSurvival RateTreatment OutcomeAppendiceal NeoplasmsOncologyColonic NeoplasmsAdenocarcinomaFemaleErratumQuinolizinesFluoroquinolonesmedicine.drugmedicine.medical_specialtyPrednisoloneEGFRDetergentsAntineoplastic AgentsAdenocarcinomaAntibodies Monoclonal HumanizedDisease-Free SurvivalMetronidazoleRashInternal medicineIntestinal NeoplasmsmedicineCombined Modality TherapyHumansSurvival rateAgedRetrospective StudiesOriginal PaperRectal Neoplasmsbusiness.industryRetrospective cohort studyAntibiotic ProphylaxisExanthemamedicine.diseaseDermatologydigestive system diseasesSurgerybusinessJournal of Cancer Research and Clinical Oncology
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