Search results for "Adenocarcinoma of Lung"

showing 10 items of 14 documents

Genome-wide profiling of non-smoking-related lung cancer cells reveals common RB1 rearrangements associated with histopathologic transformation in EG…

2020

The etiology and the molecular basis of lung adenocarcinomas (LuADs) in nonsmokers are currently unknown. Furthermore, the scarcity of available primary cultures continues to hamper our biological understanding of non-smoking-related lung adenocarcinomas (NSK-LuADs). We established patient-derived cancer cell (PDC) cultures from metastatic NSK-LuADs, including two pairs of matched EGFR-mutant PDCs before and after resistance to tyrosine kinase inhibitors (TKIs), and then performed whole-exome and RNA sequencing to delineate their genomic architecture. For validation, we analyzed independent cohorts of primary LuADs. In addition to known non-smoker-associated alterations (e.g. RET, ALK, EGFR…

0301 basic medicineLung NeoplasmsEGFRUbiquitin-Protein LigasesAdenocarcinoma of Lungmedicine.disease_cause03 medical and health sciences0302 clinical medicineGermline mutationtyrosine kinase inhibitorsmedicineGenetic predispositionHumanswhole-exome sequencingLung cancerGeneProtein Kinase InhibitorsExome sequencingMutationbusiness.industryEGFR RB1 lung adenocarcinoma nonsmokers tyrosine kinase inhibitors whole-exome sequencingHematologyrespiratory systemmedicine.diseaselung adenocarcinomadigestive system diseasesrespiratory tract diseasesErbB ReceptorsRetinoblastoma Binding Proteins030104 developmental biologyOncologyDrug Resistance Neoplasm030220 oncology & carcinogenesisCancer cellMutationCancer researchbusinessRB1Tyrosine kinaseMicrotubule-Associated Proteinsnonsmokers
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MET-EGFR dimerization in lung adenocarcinoma is dependent on EGFR mtations and altered by MET kinase inhibition

2017

Advanced lung cancer has poor survival with few therapies. EGFR tyrosine kinase inhibitors (TKIs) have high response rates in patients with activating EGFR mutations, but acquired resistance is inevitable. Acquisition of the EGFR T790M mutation causes over 50% of resistance; MET amplification is also common. Preclinical data suggest synergy between MET and EGFR inhibitors. We hypothesized that EGFR-MET dimerization determines response to MET inhibition, depending on EGFR mutation status, independently of MET copy number. We tested this hypothesis by generating isogenic cell lines from NCI-H1975 cells, which co-express L858R and T790M EGFR mutations, namely H1975L858R/T790M (EGFR TKI resista…

0301 basic medicineLung NeoplasmsKinase InhibitorsCancer Treatmentlcsh:MedicinePhysical ChemistryBiochemistryFluorophotometryT790MSpectrum Analysis Techniques0302 clinical medicineFluorescence Resonance Energy TransferMedicine and Health SciencesPhosphorylationEnzyme Inhibitorslcsh:ScienceExtracellular Signal-Regulated MAP KinasesEGFR inhibitorsStainingMice Inbred BALB CMultidisciplinaryFluorescent in Situ HybridizationPhysicsCell StainingProto-Oncogene Proteins c-metPrecipitation TechniquesErbB ReceptorsChemistryOncologySpectrophotometry030220 oncology & carcinogenesisPhysical SciencesErlotinibDimerizationProtein BindingResearch Articlemedicine.drugChemical physicsMice NudeMolecular Probe TechniquesAdenocarcinoma of LungAdenocarcinomaBiologyResearch and Analysis Methods03 medical and health sciencesGefitinibGrowth factor receptorCell Line TumormedicineAnimalsHumansImmunoprecipitationMolecular Biology TechniquesLung cancerProtein Kinase InhibitorsMolecular BiologyCell ProliferationCell growthlcsh:RReproducibility of ResultsBiology and Life SciencesDimers (Chemical physics)medicine.diseaseMolecular biologyIsogenic human disease modelsProbe Hybridizationrespiratory tract diseasesHEK293 Cells030104 developmental biologyChemical PropertiesSpecimen Preparation and TreatmentFocal Adhesion Protein-Tyrosine KinasesMutationEnzymologylcsh:QProtein MultimerizationProto-Oncogene Proteins c-aktCytogenetic TechniquesPLOS ONE
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JC Virus and Lung Adenocarcinoma: Fact or Myth?

2017

Background/aim An association has been reported between lung cancer and John Cunningham (JC) virus infection. The aim of this study was to evaluate the prevalence of JC virus in a small cohort of patients with lung adenocarcinoma and assess its presence in nodal metastasis. Materials and methods Consecutive samples of 13 surgically-removed lung tumors and 13 surrounding normal cancer-free tissues were selected. Five cases included metastatic lymph nodes. JC virus infection was assessed through nested PCR. Results Seven out of thirteen patients with lung adenocarcinoma had a positive PCR test for JC virus. One of the five patients with nodal metastasis had a positive PCR test for JC virus. N…

0301 basic medicineMaleCancer ResearchPathologymedicine.medical_specialtyTumor Virus InfectionsLung NeoplasmsvirusesJC virusAdenocarcinoma of Lung030230 surgeryAdenocarcinomamedicine.disease_causePolymerase Chain ReactionVirus03 medical and health sciences0302 clinical medicinemedicineHumansLung cancerAgedPolyomavirus InfectionsLungbusiness.industryJC Virus InfectionGeneral Medicinemedicine.diseaseJC VirusTumor Virus Infections030104 developmental biologymedicine.anatomical_structureOncologyCase-Control StudiesLymphatic MetastasisDNA ViralAdenocarcinomaFemalebusinessPolyomavirus InfectionsAnticancer research
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Lung tumorspheres reveal cancer stem cell-like properties and a score with prognostic impact in resected non-small-cell lung cancer

2019

AbstractThe high resistance against current therapies found in non-small-cell lung cancer (NSCLC) has been associated to cancer stem-like cells (CSCs), a population for which the identification of targets and biomarkers is still under development. In this study, primary cultures from early-stage NSCLC patients were established, using sphere-forming assays for CSC enrichment and adherent conditions for the control counterparts. Patient-derived tumorspheres showed self-renewal and unlimited exponential growth potentials, resistance against chemotherapeutic agents, invasion and differentiation capacities in vitro, and superior tumorigenic potential in vivo. Using quantitative PCR, gene express…

0301 basic medicineOncologyMaleCancer ResearchCellular pathologyLung NeoplasmsTumour biomarkersMice0302 clinical medicineMice Inbred NODCarcinoma Non-Small-Cell LungAged 80 and overeducation.field_of_studybiologylcsh:CytologyCancer stem cellsMiddle AgedStem-cell researchNeoplasm ProteinsGene Expression Regulation Neoplastic030220 oncology & carcinogenesisCarcinoma Squamous CellNeoplastic Stem CellsAdenocarcinomaFemaleAdultmedicine.medical_specialtyImmunologyPopulationAdenocarcinoma of LungArticle03 medical and health sciencesCellular and Molecular NeuroscienceCancer stem cellInternal medicineSpheroids CellularmedicineCarcinomaAnimalsHumanslcsh:QH573-671educationLung cancerSurvival analysisAgedbusiness.industryCD44Cell Biologymedicine.disease030104 developmental biologyA549 Cellsbiology.proteinbusinessNon-small-cell lung cancer
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Genome-Wide DNA Methylation Profiling in Early Stage I Lung Adenocarcinoma Reveals Predictive Aberrant Methylation in the Promoter Region of the Long…

2020

Introduction: Surgical procedure is the treatment of choice in early stage I lung adenocarcinoma. However, a considerable number of patients experience recurrence within the first 2 years after complete resection. Suitable prognostic biomarkers that identify patients at high risk of recurrence (who may probably benefit from adjuvant treatment) are still not available. This study aimed at identifying methylation markers for early recurrence that may become important tools for the development of new treatment modalities. Methods: Genome-wide DNA methylation profiling was performed on 30 stage I lung adenocarcinomas, comparing 14 patients with early metastatic recurrence with 16 patients with …

0301 basic medicinePulmonary and Respiratory MedicineOncologyLung adenocarcinomamedicine.medical_specialtyLung NeoplasmsADNAdenocarcinoma of LungMethylation profilingmedicine.disease_causeMethylation03 medical and health sciences0302 clinical medicinePrognostic markerPLUTInternal medicineBiomarkers TumorHumansMedicineddc:610Promoter Regions Geneticbusiness.industryHazard ratioPromoterMethylationDNADNA MethylationPrognosismedicine.diseaseLong non-coding RNA030104 developmental biologyDifferentially methylated regionsOncology030220 oncology & carcinogenesisIncRNACàncer de pulmóBiomarker (medicine)AdenocarcinomaRNA Long NoncodingNeoplasm Recurrence LocalLung cancerbusinessCarcinogenesisMetilació
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Prevalence and Clinical Outcomes for Patients With ALK-Positive Resected Stage I to III Adenocarcinoma: Results From the European Thoracic Oncology P…

2014

Purpose The prevalence of anaplastic lymphoma kinase (ALK) gene fusion (ALK positivity) in early-stage non–small-cell lung cancer (NSCLC) varies by population examined and detection method used. The Lungscape ALK project was designed to address the prevalence and prognostic impact of ALK positivity in resected lung adenocarcinoma in a primarily European population. Methods Analysis of ALK status was performed by immunohistochemistry (IHC) and fluorescent in situ hybridization (FISH) in tissue sections of 1,281 patients with adenocarcinoma in the European Thoracic Oncology Platform Lungscape iBiobank. Positive patients were matched with negative patients in a 1:2 ratio, both for IHC and for …

AdultMaleCancer Researchmedicine.medical_specialtyPathologyLung NeoplasmsPopulation610 Medicine & healthAdenocarcinoma of LungAdenocarcinomaGastroenterologyCohort Studies10049 Institute of Pathology and Molecular Pathologyhemic and lymphatic diseasesThoracic OncologyInternal medicinePrevalencemedicineHumansAnaplastic lymphoma kinase1306 Cancer ResearchAnaplastic Lymphoma KinaseLung cancereducationIn Situ Hybridization FluorescenceAgedNeoplasm Stagingeducation.field_of_studyLungbusiness.industryALK-PositiveReceptor Protein-Tyrosine KinasesMiddle Agedmedicine.diseaseImmunohistochemistryEuropeTreatment Outcomemedicine.anatomical_structureOncology10032 Clinic for Oncology and HematologyImmunohistochemistryAdenocarcinoma2730 OncologyFemalebusiness
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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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Apigenin affects leptin/leptin receptor pathway and induces cell apoptosis in lung adenocarcinoma cell line

2011

Abstract Background Apigenin, a common edible plant flavonoid, is a well characterised antioxidant. The adipokine leptin exerts proliferative and anti-apoptotic activities in a variety of cell types. In cancer cells, apigenin may induce a pro-apoptotic pathway whereas leptin has an anti-apoptotic role. The purpose of the study is to investigate the role of apigenin and of leptin/leptin receptor pathway on proliferation and on apoptosis in lung adenocarcinoma. Methods Immunocytochemistry, flow cytometry and RT-q-RT PCR, were used to investigate the expression and modulation of leptin receptors on the lung adenocarcinoma cell line A549 in presence or absence of apigenin and of leptin, alone o…

LeptinApigenin Apoptosis Leptin Lung cancerROSCancer Researchmedicine.medical_specialtyProgrammed cell deathLung NeoplasmsCell SurvivalAdipokineAdenocarcinoma of LungApoptosisCell Growth ProcessesAdenocarcinomaSettore MED/10 - Malattie Dell'Apparato RespiratorioBiologySettore BIO/09 - Fisiologiachemistry.chemical_compoundCell Line TumorInternal medicinemedicineHumansApigeninReceptorLeptin receptorCell growthLeptindigestive oral and skin physiologyEndocrinologyOncologychemistryApoptosisApigeninReceptors Leptinhormones hormone substitutes and hormone antagonistsEuropean Journal of Cancer
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Cell of origin markers identify different prognostic subgroups of lung adenocarcinoma

2018

Strong prognostic markers able to stratify lung adenocarcinoma (ADC) patients are lacking. We evaluated whether a six-immunohistochemical markers panel (TTF1, SP-A, Napsin A, MUC5AC, CDX2 and CK5), defining the putative neoplastic “cell of origin,” allows to identify prognostic subgroups among lung ADC. We screened a large cohort of ADC specimens (2003–2013) from Torino Institutional Repository identifying: (i) marker positivity by immunohistochemistry, (ii) main morphological appearance by light microscopy, (iii) presence of “hotspot” mutations of candidate genes by Sequenom technology. To evaluate possible predictors of survival and time to recurrence, uni- and multivariable-adjusted comp…

Lung adenocarcinomaMorphologyAdultMale0301 basic medicineOncologyBiomarkers; Genetic mutations; Immunohistochemistry; Lung adenocarcinoma; Morphology; Survival analysisPathologymedicine.medical_specialtyCandidate geneCell of originsix-immunohistochemical markers panel (TTF1 SP-A Napsin A MUC5AC CDX2 and CK5)Adenocarcinoma of LungKaplan-Meier Estimategenetic mutationsGene mutationBiologymedicine.disease_causeadenocarcinoma (ADC)survival analysisPathology and Forensic Medicine03 medical and health sciences0302 clinical medicineInternal medicinemorphologyBiomarkers TumormedicineHumansCDX2Survival analysisAgedbiomarkers; genetic mutations; immunohistochemistry; lung adenocarcinoma; morphology; survival analysisbiomarkersSurvival analysisMiddle Agedrespiratory systemPrognosislung adenocarcinomamedicine.diseaseImmunohistochemistryGenetic mutations030104 developmental biology030220 oncology & carcinogenesisimmunohistochemistryAdenocarcinomaImmunohistochemistryFemaleKRASBiomarkersHuman Pathology
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Nintedanib plus docetaxel after progression on immune checkpoint inhibitor therapy: insights from VARGADO, a prospective study in patients with lung …

2019

Aim: To assess outcomes in patients with advanced adenocarcinoma non-small-cell lung cancer who received nintedanib plus docetaxel after progression on prior chemotherapy followed by immune checkpoint inhibitor (ICI) therapy. Patients & methods: VARGADO is a prospective, noninterventional study. We describe initial data from a cohort of 22 patients who received nintedanib plus docetaxel after chemotherapy and ICI therapy. Results: Median progression-free survival with nintedanib plus docetaxel was 5.5 months (95% CI: 1.9–8.7 months). The objective response rate was 7/12 (58%) and the disease control rate was 10/12 (83%). Data for overall survival rate 12 months after the start of treat…

Male0301 basic medicineOncologyCancer Researchmedicine.medical_specialtyIndolesLung Neoplasmsmedicine.medical_treatmentAdenocarcinoma of LungAntineoplastic AgentsDocetaxelDisease-Free Survival03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCarcinoma Non-Small-Cell LungInternal medicineAntineoplastic Combined Chemotherapy ProtocolsmedicineClinical endpointHumansProspective StudiesLung cancerProspective cohort studyAdverse effectAgedChemotherapybusiness.industryGeneral MedicineMiddle Agedmedicine.diseaseDiscontinuationTreatment Outcome030104 developmental biologyOncologyDocetaxelchemistry030220 oncology & carcinogenesisFemaleNintedanibbusinessmedicine.drugFuture Oncology
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