Search results for " Non-Small-Cell Lung"

showing 10 items of 199 documents

Retinoic Acid affects Lung Adenocarcinoma growth by inducing differentiation via GATA6 activation and EGFR and Wnt inhibition

2016

AbstractA fundamental task in cancer research aims at the identification of new pharmacological therapies that can affect tumor growth. Differentiation therapy might exploit this function not only for hematological diseases, such as acute promyelocytic leukemia (APML) but also for epithelial tumors, including lung cancer. Here we show that Retinoic Acid (RA) arrests in vitro and in vivo the growth of Tyrosine Kinase Inhibitors (TKI) resistant Non Small Cell Lung Cancer (NSCLC). In particular, we found that RA induces G0/G1 cell cycle arrest in TKI resistant NSCLC cells and activates terminal differentiation programs by modulating the expression of GATA6, a key transcription factor involved …

0301 basic medicineAcute promyelocytic leukemiaScienceEGFRRetinoic acidMice NudeTretinoinBiologyArticle03 medical and health scienceschemistry.chemical_compoundDifferentiation therapySettore BIO/13 - Biologia ApplicataCarcinoma Non-Small-Cell LungCell Line TumorGATA6 Transcription FactormedicineRetinoic acidAnimalsHumansLung cancerProtein Kinase InhibitorsWnt Signaling PathwayTranscription factorCell ProliferationMultidisciplinaryQRWnt signaling pathwayCell Differentiationmedicine.diseaseG1 Phase Cell Cycle CheckpointsXenograft Model Antitumor Assaysrespiratory tract diseasesErbB Receptorslung cancerAnimals; Carcinoma Non-Small-Cell Lung; Cell Differentiation; Cell Line Tumor; Cell Proliferation; Drug Resistance Neoplasm; ErbB Receptors; G1 Phase Cell Cycle Checkpoints; GATA6 Transcription Factor; Humans; Mice Nude; Protein Kinase Inhibitors; Signal Transduction; Tretinoin; Wnt Signaling Pathway; Xenograft Model Antitumor Assays030104 developmental biologychemistryDrug Resistance NeoplasmImmunologyCancer researchMedicineAdenocarcinomaEngineering sciences. TechnologyTyrosine kinaseSignal Transduction
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Targeting prohibitins with chemical ligands inhibits KRAS-mediated lung tumours.

2017

KRAS is one of the most frequently mutated oncogenes in human non-small cell lung cancers (NSCLCs). RAS proteins trigger multiple effector signalling pathways including the highly conserved RAF-MAPK pathway. CRAF, a direct RAS effector protein, is required for KRAS-mediated tumourigenesis. Thus, the molecular mechanisms driving the activation of CRAF are intensively studied. Prohibitin 1 (PHB1) is an evolutionarily conserved adaptor protein and interaction of CRAF with PHB1 at the plasma membrane is essential for CRAF activation. Here, we demonstrate that PHB1 is highly expressed in NSCLC patients and correlates with poor survival. Targeting of PHB1 with two chemical ligands (rocaglamide an…

0301 basic medicineCancer ResearchEGF Family of ProteinsLung NeoplasmsBiologyLigandsProto-Oncogene Proteins p21(ras)03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineGrowth factor receptorRocaglamideEpidermal growth factorCarcinoma Non-Small-Cell LungCell Line TumorProhibitinsGeneticsAnimalsHumansMolecular Targeted TherapyProhibitinMolecular BiologyBenzofuransCell ProliferationRas InhibitorMice KnockoutTNF Receptor-Associated Factor 3EffectorXenograft Model Antitumor Assaysrespiratory tract diseasesCell biologyProto-Oncogene Proteins p21(ras)Gene Expression Regulation NeoplasticRepressor Proteins030104 developmental biologychemistry030220 oncology & carcinogenesisras Proteinsraf KinasesSignal transductionSignal TransductionOncogene
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NGS‐based liquid biopsy profiling identifies mechanisms of resistance to ALK inhibitors: a step toward personalized NSCLC treatment

2021

Despite impressive and durable responses, nonsmall cell lung cancer (NSCLC) patients treated with anaplastic lymphoma kinase (ALK) inhibitors (ALK‐Is) ultimately progress due to development of resistance. Here, we have evaluated the clinical utility of circulating tumor DNA (ctDNA) profiling by next‐generation sequencing (NGS) upon disease progression. We collected 26 plasma and two cerebrospinal fluid samples from 24 advanced ALK‐positive NSCLC patients at disease progression to an ALK‐I. These samples were analyzed by NGS and digital PCR. A tool to retrieve variants at the ALK locus was developed (VALK tool). We identified at least one resistance mutation in the ALK locus in ten (38.5%) p…

0301 basic medicineCancer ResearchLung NeoplasmsEML4-ALKAntineoplastic AgentsEML4‐ALKmedicine.disease_causeNSCLCIDH2Circulating Tumor DNA03 medical and health sciencesALK-TKI0302 clinical medicineCarcinoma Non-Small-Cell LungMAP2K1hemic and lymphatic diseasesALK‐TKIGeneticsmedicineHumansAnaplastic lymphoma kinaseAnaplastic Lymphoma KinaseDigital polymerase chain reactionPrecision MedicineLiquid biopsyProtein Kinase InhibitorsneoplasmsResearch ArticlesRC254-282MutationCrizotinibliquid biopsybusiness.industryHigh-Throughput Nucleotide SequencingNeoplasms. Tumors. Oncology. Including cancer and carcinogensGeneral MedicineResistance mutation3. Good health030104 developmental biologyOncologyDrug Resistance Neoplasm030220 oncology & carcinogenesisNGSMutationCancer researchMolecular MedicinebusinessResearch Articlemedicine.drugMolecular Oncology
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Immunotherapy in non-small-cell lung cancer: a bridge between research and clinical practice

2018

Lung cancer has been historically considered a poorly immunogenic disease because of the few evidence of immune responses in affected patients and the limited efficacy of immunomodulating strategies. Recent understanding of the molecular mechanisms leading to cancer immune evasion has allowed the development of a new class of drugs called immune checkpoint inhibitors, which reactivate host responses with outstanding clinical benefits in a portion of patients with non-small-cell lung cancer. In this review, we briefly summarize the basis of immunogenicity and immune escape of cancer, with specific focus on non-small-cell lung cancer, mechanisms underlying immune checkpoint inhibitors effica…

0301 basic medicineCancer ResearchLung NeoplasmsSettore MED/06 - Oncologia Medicamedicine.medical_treatmentProgrammed Cell Death 1 Receptorimmune checkpoint inhibitorDiseaseNSCLCBioinformaticsB7-H1 Antigenimmune checkpoint inhibitorsTranslational Research Biomedical0302 clinical medicineCarcinoma Non-Small-Cell LungPD-1clinical studiesNSCLC; PD-1; PD-L1; biomarkers; cancer immunogenicity; clinical studies; immune checkpoint inhibitors; translational researchMolecular Targeted TherapybiologyImmunogenicityGeneral Medicinecancer immunogenicityOncology030220 oncology & carcinogenesisbiomarkerCytokinesImmunotherapyPD-L1chemical and pharmacologic phenomena03 medical and health sciencesLymphocytes Tumor-InfiltratingImmune systemPD-L1Biomarkers TumormedicineHumansLung cancerbusiness.industryImmunitybiomarkersCancerImmunotherapymedicine.disease030104 developmental biologytranslational researchTumor EscapeMutationbiology.proteinTumor Escapebusinessclinical studieFuture Oncology
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Cyclic pentapeptide cRGDfK enhances the inhibitory effect of sunitinib on TGF-β1-induced epithelial-to-mesenchymal transition in human non-small cell…

2020

AbstractIn human lung cancer progression, the EMT process is characterized by the transformation of cancer cells into invasive forms that migrate to other organs. Targeting to EMT-related molecules is emerging as a novel therapeutic approach for the prevention of lung cancer cell migration and invasion. Traf2- and Nck-interacting kinase (TNIK) has recently been considered as an anti-proliferative target molecule to regulate the Wnt signaling pathway in several types of cancer cells. In the present study, we evaluated the inhibitory effect of a tyrosine kinase inhibitor sunitinib and the integrin-αVβ3targeted cyclic peptide (cRGDfK) on EMT in human lung cancer cells. Sunitinib strongly inhib…

0301 basic medicineCell signalingIntegrinsLung NeoplasmsProtein ExpressionCancer TreatmentSmad ProteinsSignal transductionLung and Intrathoracic TumorsTyrosine-kinase inhibitorAdenosine Triphosphate0302 clinical medicineCarcinoma Non-Small-Cell LungCatalytic DomainAntineoplastic Combined Chemotherapy ProtocolsMedicine and Health SciencesSunitinibWnt Signaling PathwayWNT Signaling CascadeMultidisciplinarySunitinibChemistryQRWnt signaling pathwaySignaling cascadesDrug SynergismExtracellular MatrixMolecular Docking SimulationOncology030220 oncology & carcinogenesisMedicineCellular Structures and OrganellesSignal transductionResearch Articlemedicine.drugCell biologySignal InhibitionEpithelial-Mesenchymal TransitionCell Survivalmedicine.drug_classScienceSMAD signalingProtein Serine-Threonine KinasesResearch and Analysis MethodsPeptides CyclicTransforming Growth Factor beta103 medical and health sciencesCell Line TumorGene Expression and Vector TechniquesCell AdhesionBiomarkers TumormedicineHumansNeoplasm InvasivenessEpithelial–mesenchymal transitionMolecular Biology TechniquesLung cancerMolecular BiologyA549 cellMolecular Biology Assays and Analysis TechniquesBiology and life sciencesCancers and NeoplasmsIntegrin alphaVbeta3medicine.diseaseNon-Small Cell Lung Cancer030104 developmental biologyTGF-beta signaling cascadeA549 CellsTNIKCancer cellCancer researchPLOS ONE
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Serum metabolomic profiling facilitates the non-invasive identification of metabolic biomarkers associated with the onset and progression of non-smal…

2016

Lung cancer (LC) is responsible for most cancer deaths. One of the main factors contributing to the lethality of this disease is the fact that a large proportion of patients are diagnosed at advanced stages when a clinical intervention is unlikely to succeed. In this study, we evaluated the potential of metabolomics by H-1-NMR to facilitate the identification of accurate and reliable biomarkers to support the early diagnosis and prognosis of non-small cell lung cancer (NSCLC). We found that the metabolic profile of NSCLC patients, compared with healthy individuals, is characterized by statistically significant changes in the concentration of 18 metabolites representing different amino acids…

0301 basic medicineGerontologyOncologyAdultMalemedicine.medical_specialtyLung NeoplasmsProton Magnetic Resonance SpectroscopyDiseaseNSCLC03 medical and health sciences0302 clinical medicineMetabolomicsInternal medicineCarcinoma Non-Small-Cell LungmedicineBiomarkers TumorHumansLung cancerAgedbusiness.industryNon invasivebiomarkersLipid metabolismMiddle Agedmedicine.diseasemetabolomicsPathophysiology030104 developmental biologyMetabolomic profilingOncology030220 oncology & carcinogenesisDisease ProgressionFemaleNon small cellprognosisbusinessResearch Paperearly diagnosis
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Amphiregulin contained in NSCLC-exosomes induces osteoclast differentiation through the activation of EGFR pathway

2017

AbstractNon-small cell lung cancer (NSCLC) remains the leading cause of cancer-related deaths worldwide. The majority of patients are diagnosed in advanced disease stage. Bone metastasis is the most frequent complication in NSCLC resulting in osteolytic lesions. The perfect balance between bone-resorbing osteoclasts and bone-forming osteoblasts activity is lost in bone metastasis, inducing osteoclastogenesis. In NSCLC, the epidermal growth factor receptor (EGFR) pathway is constitutively activated. EGFR binds Amphiregulin (AREG) that is overexpressed in several cancers such as colon, breast and lung. Its levels in plasma of NSCLC patients correlate with poor prognosis and AREG was recently …

0301 basic medicineLung NeoplasmsCellular differentiationAmphiregulin exosomes NSCLC EGFROsteoclastsExosomes NSCLC AmphiregulinNSCLCExosomesMice0302 clinical medicineSettore BIO/13 - Biologia ApplicataCarcinoma Non-Small-Cell LungMedicineEpidermal growth factor receptorRNA Small InterferingMultidisciplinarybiologyQProteolytic enzymesRBone metastasisCell Differentiation3. Good healthErbB ReceptorsGene Expression Regulation Neoplasticmedicine.anatomical_structureRANKL030220 oncology & carcinogenesisMedicineEngineering sciences. TechnologySciencePrimary Cell CultureBone NeoplasmsAmphiregulinArticle03 medical and health sciencesAmphiregulinOsteoclastCell Line TumorAnimalsHumansbusiness.industryRANK LigandBiological Transportmedicine.diseaseMicrovesiclesCoculture Techniquesrespiratory tract diseases030104 developmental biologyRAW 264.7 CellsImmunologybiology.proteinCancer researchbusiness
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PARP inhibition enhances tumor cell-intrinsic immunity in ERCC1-deficient non-small cell lung cancer.

2018

The cyclic GMP-AMP synthase/stimulator of IFN genes (cGAS/STING) pathway detects cytosolic DNA to activate innate immune responses. Poly(ADP-ribose) polymerase inhibitors (PARPi) selectively target cancer cells with DNA repair deficiencies such as those caused by BRCA1 mutations or ERCC1 defects. Using isogenic cell lines and patient-derived samples, we showed that ERCC1-defective non-small cell lung cancer (NSCLC) cells exhibit an enhanced type I IFN transcriptomic signature and that low ERCC1 expression correlates with increased lymphocytic infiltration. We demonstrated that clinical PARPi, including olaparib and rucaparib, have cell-autonomous immunomodulatory properties in ERCC1-defecti…

0301 basic medicineLung NeoplasmsDNA repairPoly (ADP-Ribose) Polymerase-1Triple Negative Breast NeoplasmsPoly(ADP-ribose) Polymerase InhibitorsPoly (ADP-Ribose) Polymerase InhibitorB7-H1 AntigenOlaparib03 medical and health scienceschemistry.chemical_compoundInterferon-gamma0302 clinical medicinePARP1Carcinoma Non-Small-Cell LungHumansRucaparibA549 cellChemistryBRCA1 ProteinMembrane ProteinsGeneral MedicineEndonucleasesIsogenic human disease modelsNucleotidyltransferasesDNA-Binding Proteins030104 developmental biologyA549 Cells030220 oncology & carcinogenesisCancer cellCancer researchFemaleResearch ArticleThe Journal of clinical investigation
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Profile of the Roche cobas® EGFR mutation test v2 for non-small cell lung cancer

2017

Abstract: Introduction: The discovery of driver mutations in non-small cell lung cancer (NSCLC) has led to the development of genome-based personalized medicine. Fifteen to 20% of adenocarcinomas harbor an epidermal growth factor receptor (EGFR) activating mutation associated with responses to EGFR tyrosine kinase inhibitors (TKIs). Individual laboratories' expertise and the availability of appropriate equipment are valuable assets in predictive molecular pathology, although the choice of methods should be determined by the nature of the samples to be tested and whether the detection of only well-characterized EGFR mutations or rather, of all detectable mutations, is required.Areas covered:…

0301 basic medicineLung NeoplasmsEGFRDNA Mutational Analysis2734Real-Time Polymerase Chain Reactionmedicine.disease_causeBioinformaticsGenomePathology and Forensic Medicineresistance03 medical and health sciences0302 clinical medicineCarcinoma Non-Small-Cell LungGeneticsHumansMedicineEpidermal growth factor receptorLiquid biopsyLung cancerMolecular Biologycobas®Mutationliquid biopsybiologyReverse Transcriptase Polymerase Chain Reactionbusiness.industryMolecular pathologymedicine.diseaseTKIErbB Receptors030104 developmental biology030220 oncology & carcinogenesisCancer researchbiology.proteinMolecular Medicinecompanion diagnosticHuman medicineReagent Kits DiagnosticPersonalized medicinemutationbusinessCompanion diagnosticExpert Review of Molecular Diagnostics
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Central nervous system involvement in ALK-rearranged NSCLC : promising strategies to overcome crizotinib resistance

2016

ABSTRACT: Introduction: ALK rearranged Non Small Cell Lung Cancers (NSCLCs) represent a distinct subgroup of patients with peculiar clinic-pathological features. These patients exhibit dramatic responses when treated with the ALK tyrosine kinase inhibitor Crizotinib, albeit Central Nervous System (CNS) activity is much less impressive than that observed against extracranial lesions. CNS involvement has become increasingly observed in these patients, given their prolonged survival. Several novel generation ALK inhibitors have been developing to increase CNS penetration and to provide more complete ALK inhibition. Areas covered: The CNS activity of Crizotinib and novel generation ALK inhibito…

0301 basic medicineLung NeoplasmsSettore MED/06 - Oncologia MedicaPyridinesPyridineDrug ResistanceNSCLCTyrosine-kinase inhibitorALK translocations Brain metastases central nervous system metastases leptomeningeal metastases NSCLC Animals Antineoplastic Agents Brain Neoplasms Carcinoma Non-Small-Cell Lung Drug Design Drug Resistance Neoplasm Gene Rearrangement Humans Lung Neoplasms Protein Kinase Inhibitors Pyrazoles Pyridines Receptor Protein-Tyrosine Kinases Oncology Pharmacology (medical)Cns penetrationAntineoplastic Agent0302 clinical medicinecentral nervous system metastasesCarcinoma Non-Small-Cell Lunghemic and lymphatic diseasesMedicinePharmacology (medical)Anaplastic Lymphoma Kinaseleptomeningeal metastaseNon-Small-Cell LungGene RearrangementBrain NeoplasmsReceptor Protein-Tyrosine Kinasemedicine.anatomical_structureOncology030220 oncology & carcinogenesisNon small cellHumanmedicine.drugBrain metastasemedicine.drug_classCentral nervous systemProtein Kinase InhibitorCNS InvolvementAntineoplastic AgentsALK translocationBrain Neoplasm03 medical and health sciencesCrizotinibAnimalsHumansCns activityCrizotinib resistanceProtein Kinase Inhibitorsleptomeningeal metastasescentral nervous system metastaseCrizotinibAnimalbusiness.industryCarcinomaReceptor Protein-Tyrosine KinasesBrain metastasesLung Neoplasm030104 developmental biologyALK translocationsDrug Resistance NeoplasmDrug DesignPyrazoleImmunologyCancer researchNeoplasmPyrazolesHuman medicinebusinessExpert review of anticancer therapy
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