Search results for "neoplastic"

showing 10 items of 2901 documents

PHD3 Controls Lung Cancer Metastasis and Resistance to EGFR Inhibitors through TGFα.

2018

Abstract Lung cancer is the leading cause of cancer-related death worldwide, in large part due to its high propensity to metastasize and to develop therapy resistance. Adaptive responses to hypoxia and epithelial–mesenchymal transition (EMT) are linked to tumor metastasis and drug resistance, but little is known about how oxygen sensing and EMT intersect to control these hallmarks of cancer. Here, we show that the oxygen sensor PHD3 links hypoxic signaling and EMT regulation in the lung tumor microenvironment. PHD3 was repressed by signals that induce EMT and acted as a negative regulator of EMT, metastasis, and therapeutic resistance. PHD3 depletion in tumors, which can be caused by the EM…

0301 basic medicineCancer ResearchEpithelial-Mesenchymal TransitionLung NeoplasmsMice NudeAntineoplastic AgentsSMADDrug resistanceMetastasisHypoxia-Inducible Factor-Proline DioxygenasesMitochondrial Proteins03 medical and health sciencesErlotinib HydrochlorideMice0302 clinical medicineDownregulation and upregulationCell Line TumorTumor MicroenvironmentMedicineAnimalsHumansNeoplasm MetastasisLung cancerProtein Kinase InhibitorsEGFR inhibitorsbusiness.industryIntracellular Signaling Peptides and ProteinsCancerTransforming Growth Factor alphamedicine.diseaseHCT116 CellsXenograft Model Antitumor AssaysCell HypoxiaErbB Receptors030104 developmental biologyOncologyA549 CellsDrug Resistance Neoplasm030220 oncology & carcinogenesisembryonic structuresCancer researchFemaleErlotinibbusinessApoptosis Regulatory Proteinsmedicine.drugCancer research
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Transcriptional profiling of circulating tumor cells in multiple myeloma: a new model to understand disease dissemination

2020

The reason why a few myeloma cells egress from the bone marrow (BM) into peripheral blood (PB) remains unknown. Here, we investigated molecular hallmarks of circulating tumor cells (CTCs) to identify the events leading to myeloma trafficking into the bloodstream. After using next-generation flow to isolate matched CTCs and BM tumor cells from 32 patients, we found high correlation in gene expression at single-cell and bulk levels (r ≥ 0.94, P = 10−16), with only 55 genes differentially expressed between CTCs and BM tumor cells. CTCs overexpressed genes involved in inflammation, hypoxia, or epithelial–mesenchymal transition, whereas genes related with proliferation were downregulated in CTCs…

0301 basic medicineCancer ResearchEpithelial-Mesenchymal TransitionTranscription GeneticGene ExpressionBiologycirculating tumor cell03 medical and health sciences0302 clinical medicineCirculating tumor cellBone MarrowCell MovementCancer stem cellCell Line TumorTumor MicroenvironmentmedicineHumansHypoxiaMultiple myelomaCell ProliferationInflammationGene knockdownliquid biopsyCD44CENPFHematologyNeoplastic Cells CirculatingPrognosismedicine.disease3. Good healthmultiple myeloma030104 developmental biologymedicine.anatomical_structureOncologyCell culture030220 oncology & carcinogenesisNeoplastic Stem CellsCancer researchbiology.proteinBone marrow
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Tumour mutational burden as a biomarker for immunotherapy: Current data and emerging concepts

2020

International audience; Treatment with immune checkpoint inhibitors targeting programmed cell death protein 1 (PD-1) or its ligand (PD-L1) can generate durable responses in various cancer types, but only in a subset of patients. The use of predictive biomarkers for response to PD-1/PD-L1 inhibitors is critical for patient selection. Expression of PD-L1 has demonstrated utility in patient selection. Tumour mutational burden (TMB) is an emerging biomarker for response to PD-1/PD-L1 inhibitors. The evaluation of this biomarker is based on the hypothesis that a high number of mutations in somatic exonic regions will lead to an increase in neoantigen production, which could then be recognised by…

0301 basic medicineCancer ResearchImmune checkpoint inhibitorsmedicine.medical_treatment[SDV]Life Sciences [q-bio]DNA Mutational AnalysisProgrammed Cell Death 1 ReceptorTumour mutational burdenBioinformaticsArticleB7-H1 Antigen03 medical and health sciencesAntineoplastic Agents Immunological0302 clinical medicineImmune systemNeoplasmsBiomarkers TumorHumansMedicineIn patientGenetic TestingPredictive biomarkerbusiness.industryPatient SelectionCancerBiomarkerImmunotherapymedicine.disease3. Good healthBiomarker (cell)[SDV] Life Sciences [q-bio]030104 developmental biologyOncologyDrug Resistance Neoplasm030220 oncology & carcinogenesisMutationImmunotherapybusinessCD8
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9-ING-41, a small-molecule glycogen synthase kinase-3 inhibitor, is active in neuroblastoma.

2018

Advanced stage neuroblastoma is a very aggressive pediatric cancer with limited treatment options and a high mortality rate. Glycogen Synthase Kinase-3β (GSK-3β) is a potential therapeutic target in neuroblastoma. Using immunohistochemical staining, we observed positive GSK-3β expression in 67% of human neuroblastomas (34 out of 51 cases). Chemically distinct GSK-3 inhibitors (AR-A014418, TDZD8 and 9-ING-41), suppressed the growth of neuroblastoma cells whereas 9-ING-41, a clinically relevant small molecule GSK-3β inhibitor with broad spectrum pre-clinical antitumor activity, being the most potent. Inhibition of GSK-3 resulted in a decreased expression of the antiapoptotic molecule XIAP and…

0301 basic medicineCancer ResearchIndolesMice NudeCell Growth ProcessesIrinotecanArticleMaleimides03 medical and health sciencesMiceNeuroblastoma0302 clinical medicineGSK-3NeuroblastomaCell Line TumorAntineoplastic Combined Chemotherapy ProtocolsmedicineAnimalsHumansPharmacology (medical)Enzyme InhibitorsGlycogen synthasePharmacologyGlycogen Synthase Kinase 3 betabiologyChemistryDrug Synergismmedicine.diseasePediatric cancerXenograft Model Antitumor AssaysXIAP030104 developmental biologyOncologyCell cultureApoptosis030220 oncology & carcinogenesisCancer researchbiology.proteinImmunohistochemistryFemaleAnti-cancer drugs
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Doxorubicin anti-tumor mechanisms include Hsp60 post-translational modifications leading to the Hsp60/p53 complex dissociation and instauration of re…

2017

Hsp60 is a pro-carcinogenic chaperonin in certain tumor types by interfering with apoptosis and with tumor cell death. In these tumors, it is not known whether or not doxorubicin anti-tumor effects include a blockage of the pro-carcinogenic action of this protein. We used the human lung mucoepidermoid cell line NCI-H292 and different doses of doxorubicin to measure cell viability, cell cycle progression, cell senescence indicators, Hsp60 levels and its post-translational modifications as well as the release of the chaperonin into the extracellular environment. Cell viability was reduced in relation to doxorubicin dose and this was paralleled by the appearance of cell senescence markers. Con…

0301 basic medicineCancer ResearchLung NeoplasmsChaperoninsCellApoptosismedicine.disease_causeHistones0302 clinical medicineCellular SenescenceAntibiotics AntineoplasticAcetylationG2 Phase Cell Cycle Checkpointsmedicine.anatomical_structureOncology030220 oncology & carcinogenesisCell agingIntracellularProtein BindingSignal TransductionSenescenceCyclin-Dependent Kinase Inhibitor p21animal structuresCell Survivalchemical and pharmacologic phenomenaBiologycomplex mixturesMitochondrial ProteinsDoxorubicin Hsp60 Acetylation Ubiquitination p53 Replicative senescence03 medical and health sciencesDoxorubicin; Hsp60; p53; replicative senescence; post-translational modificationsCell Line TumormedicineHumansCell Proliferationdoxorubicin p53 Hsp60Dose-Response Relationship DrugCell growthfungiUbiquitinationChaperonin 60Molecular biology030104 developmental biologyAcetylationApoptosisDoxorubicinProteolysisCancer researchCarcinoma MucoepidermoidTumor Suppressor Protein p53CarcinogenesisProtein Processing Post-Translational
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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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The PDGFRβ/ERK1/2 pathway regulates CDCP1 expression in triple-negative breast cancer

2018

Background CDCP1, a transmembrane protein with tumor pro-metastatic activity, was recently identified as a prognostic marker in TNBC, the most aggressive breast cancer subtype still lacking an effective molecular targeted therapy. The mechanisms driving CDCP1 over-expression are not fully understood, although several stimuli derived from tumor microenvironment, such as factors present in Wound Healing Fluids (WHFs), reportedly increase CDCP1 levels. Methods The expression of CDCP1, PDGFRβ and ERK1/2cell was tested by Western blot after stimulation of MDA-MB-231 cells with PDGF-BB and, similarly, in presence or not of ERK1/2 inhibitor in a panel of TNBC cell lines. Knock-down of PDGFRβ was e…

0301 basic medicineCancer ResearchMAP Kinase Signaling SystemCDCP1medicine.medical_treatmentPDGFRβPDGF-BBBecaplerminTriple Negative Breast NeoplasmsBiologylcsh:RC254-282Targeted therapyReceptor Platelet-Derived Growth Factor beta03 medical and health sciences0302 clinical medicineFISHDownregulation and upregulationWestern blotAntigens CDAntigens NeoplasmCell Line TumorGeneticsmedicineHumansRNA Small InterferingReceptorTriple-negative breast cancerMitogen-Activated Protein Kinase 1Tumor microenvironmentMitogen-Activated Protein Kinase 3ERK1/2medicine.diagnostic_testMiddle Agedlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensNeoplasm ProteinsUp-RegulationGene Expression Regulation Neoplastic030104 developmental biologyOncologyGene Knockdown Techniques030220 oncology & carcinogenesisCDCP1Cancer researchImmunohistochemistryFemaleCell Adhesion MoleculesTNBCResearch ArticleIHCBMC Cancer
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Dual Constant Domain-Fab: A novel strategy to improve half-life and potency of a Met therapeutic antibody

2016

The kinase receptor encoded by the Met oncogene is a sensible target for cancer therapy. The chimeric monovalent Fab fragment of the DN30 monoclonal antibody (MvDN30) has an odd mechanism of action, based on cell surface removal of Met via activation of specific plasma membrane proteases. However, the short half-life of the Fab, due to its low molecular weight, is a severe limitation for the deployment in therapy. This issue was addressed by increasing the Fab molecular weight above the glomerular filtration threshold through the duplication of the constant domains, in tandem (DCD-1) or reciprocally swapped (DCD-2). The two newly engineered molecules showed biochemical properties comparable…

0301 basic medicineCancer ResearchMice SCIDCancer targeted therapy0302 clinical medicineMice Inbred NODEpidermal growth factor receptorPhosphorylationbiologyChemistryImmunoglobulin Fab FragmentsAntibodies MonoclonalGeneral MedicineArticlesProto-Oncogene Proteins c-metHalf-lifeCell biologyOncology030220 oncology & carcinogenesisColonic NeoplasmsMetMolecular MedicineFemalemedicine.symptomSignal transductionAntibodySignal Transductionmedicine.drug_classColonAntibody; Cancer targeted therapy; Fab; Half-life; Met; Protein engineering; Cancer Research; Genetics; Molecular MedicineAntineoplastic AgentsMonoclonal antibody03 medical and health sciencesImmunoglobulin Fab FragmentsProtein DomainsCell Line TumormedicineGeneticsAnimalsHumansFabAntibodyCell growthMolecular biology030104 developmental biologyHEK293 CellsMechanism of actionHepatocyte Growth Factor ReceptorA549 Cellsbiology.proteinProtein engineering
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DNA methylation of shelf, shore and open sea CpG positions distinguish high microsatellite instability from low or stable microsatellite status colon…

2019

Aim: To investigate the genome-wide methylation of genetically characterized colorectal cancer stem cell (CR-CSC) lines. Materials & methods: Eight CR-CSC lines were isolated from primary colorectal cancer (CRC) tissues, cultured and characterized for aneuploidy, mutational status of CRC-related genes and microsatellite instability (MSI). Genome-wide DNA methylation was assessed by MethylationEPIC microarray. Results: We describe a distinctive methylation pattern that is maintained following in vivo passages in immune-compromised mice. We identified an epigenetic CR-CSC signature associated with MSI. We noticed that the preponderance of the differentially methylated positions do not re…

0301 basic medicineCancer ResearchMicroarrayColorectal cancercolon cancer stem cellsSocio-culturaleBiologyEpigenesis Genetic03 medical and health sciencesMice0302 clinical medicineGeneticsmedicineAnimalsHumansEpigeneticsneoplasmsMSIMSSMicrosatellite instabilityMethylationcolon cancer stem cells DNA methylation MSI MSSDNA Methylationmedicine.diseasedigestive system diseases030104 developmental biologyCpG siteDrug Resistance Neoplasm030220 oncology & carcinogenesisDNA methylationColonic NeoplasmsCancer researchNeoplastic Stem CellsMicrosatelliteHeterograftsCpG IslandsMicrosatellite Instabilitycolon cancer stem cellEpigenomics
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Transcriptional Profiles and Stromal Changes Reveal Bone Marrow Adaptation to Early Breast Cancer in Association with Deregulated Circulating microRN…

2020

Abstract The presence of a growing tumor establishes a chronic state of inflammation that acts locally and systemically. Bone marrow responds to stress signals by expanding myeloid cells endowed with immunosuppressive functions, further fostering tumor growth and dissemination. How early in transformation the cross-talk with the bone marrow begins and becomes detectable in blood is unknown. Here, gene expression profiling of the bone marrow along disease progression in a spontaneous model of mammary carcinogenesis demonstrates that transcriptional modifications in the hematopoietic compartment occurred as early as preinvasive disease stages. The transcriptional profile showed downregulation…

0301 basic medicineCancer ResearchMyeloidStromal cellInflammationApoptosisBreast NeoplasmsBiologySettore MED/08 - Anatomia PatologicaCXCR403 medical and health sciencesMice0302 clinical medicineBone MarrowmedicineBiomarkers TumorTumor Cells CulturedAnimalsHumansCirculating MicroRNACell ProliferationMice Inbred BALB CInnate immune systemGene Expression ProfilingAcquired immune systemAdaptation PhysiologicalXenograft Model Antitumor AssaysGene Expression Regulation NeoplasticHaematopoiesis030104 developmental biologymedicine.anatomical_structureOncologyTrascriptional profiles early brest cancer microRNAs030220 oncology & carcinogenesisCancer researchFemaleBone marrowmedicine.symptomStromal CellsTranscriptomeCancer research
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