Search results for "Neoplasms"

showing 10 items of 7988 documents

Insulin Resistance in PCOS Patients Enhances Oxidative Stress and Leukocyte Adhesion: Role of Myeloperoxidase

2016

Cardiovascular diseases and oxidative stress are related to polycystic ovary syndrome (PCOS) and insulin resistance (IR). We have evaluated the relationship between myeloperoxidase (MPO) and leukocyte activation in PCOS patients according to homeostatic model assessment of IR (HOMA-IR), and have explored a possible correlation between these factors and endocrine and inflammatory parameters. This was a prospective controlled study conducted in an academic medical center. The study population consisted of 101 PCOS subjects and 105 control subjects. We divided PCOS subjects into PCOS non-IR (HOMA-IR2.5). Metabolic and anthropometric parameters, total and mitochondrial reactive oxygen species (…

0301 basic medicineMitochondrial ROSendocrine system diseasesmedicine.medical_treatment030204 cardiovascular system & hematologyPathology and Laboratory Medicinemedicine.disease_causeBiochemistryWhite Blood CellsFluorescence MicroscopyEndocrinology0302 clinical medicineAnimal CellsMedicine and Health SciencesLeukocytesInsulinImmune ResponseEnergy-Producing OrganellesMicroscopyMultidisciplinaryQRLight MicroscopyPolycystic ovaryMitochondriaOncologyMyeloperoxidaseHomeostatic model assessmentCytokinesMedicineFemaleCellular TypesCellular Structures and OrganellesInflammation MediatorsResearch ArticlePolycystic Ovary SyndromeAdultmedicine.medical_specialtyAdhesion MoleculesImmune CellsScienceImmunologyBioenergeticsBiologyResearch and Analysis MethodsProinflammatory cytokineYoung Adult03 medical and health sciencesSigns and SymptomsInsulin resistanceDiagnostic MedicineInternal medicineCell AdhesionmedicineHumansPeroxidaseInflammationDiabetic EndocrinologyBlood CellsInsulinBiology and Life SciencesCancers and Neoplasmsnutritional and metabolic diseasesCell BiologyMolecular Developmentmedicine.diseaseHormonesOxidative Stress030104 developmental biologyEndocrinologybiology.proteinInsulin ResistanceReactive Oxygen SpeciesGynecological TumorsOxidative stressDevelopmental Biology
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Oncogenic Deregulation of EZH2 as an Opportunity for Targeted Therapy in Lung Cancer.

2016

Abstract As a master regulator of chromatin function, the lysine methyltransferase EZH2 orchestrates transcriptional silencing of developmental gene networks. Overexpression of EZH2 is commonly observed in human epithelial cancers, such as non–small cell lung carcinoma (NSCLC), yet definitive demonstration of malignant transformation by deregulated EZH2 remains elusive. Here, we demonstrate the causal role of EZH2 overexpression in NSCLC with new genetically engineered mouse models of lung adenocarcinoma. Deregulated EZH2 silences normal developmental pathways, leading to epigenetic transformation independent of canonical growth factor pathway activation. As such, tumors feature a transcrip…

0301 basic medicineModels MolecularLung Neoplasmsmedicine.medical_treatmentMolecular ConformationGene ExpressionAntineoplastic Agentsmacromolecular substancesBiologymedicine.disease_causeArticleMalignant transformationTargeted therapy03 medical and health sciencesMiceStructure-Activity RelationshipCell Line TumormedicineAnimalsHumansEnhancer of Zeste Homolog 2 ProteinMolecular Targeted TherapyLung cancerPromoter Regions GeneticGene Expression ProfilingEZH2Cancermedicine.diseaseMagnetic Resonance ImagingXenograft Model Antitumor AssaysChromatinrespiratory tract diseasesGene Expression Regulation NeoplasticDisease Models Animal030104 developmental biologyCell Transformation NeoplasticEnhancer Elements GeneticOncologyDrug DesignCancer researchAdenocarcinomaKRASEpigenetic therapyCancer discovery
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1,3,5-Triazines: A promising scaffold for anticancer drugs development

2017

This review covering literature reports from the beginning of this century to 2016 describes the synthetic pathways, the antitumor activity, the structure-activity relationship and, whenever reported, the possible mechanism of action of 1,3,5-triazine derivatives as well as of their hetero-fused compounds. Many 1,3,5-triazine derivatives, both uncondensed and hetero-fused, have shown remarkable antitumor activities and some of them reached clinical development.

0301 basic medicineModels MolecularScaffold31Disubstituted 135-triazineTrisubstituted 135-triazineAntineoplastic AgentsChemistry Techniques Synthetic01 natural sciences03 medical and health sciencesStructure-Activity RelationshipNeoplasmsDrug DiscoverymedicineAnimalsHumans5-TriazinesTrisubstituted 1Disubstituted 1Antitumor activityPharmacologyHeterofused 135-triazine010405 organic chemistryChemistryTriazinesNitrogen heterocyclesDrug Discovery3003 Pharmaceutical ScienceOrganic ChemistryGeneral MedicineHeterofused 1Combinatorial chemistry135-Triazine0104 chemical sciences030104 developmental biologyNitrogen heterocycleMechanism of action1; 3; 5-Triazines; Antitumor activity; Disubstituted 1; 3; 5-triazines; Heterofused 1; 3; 5-triazines; Nitrogen heterocycles; Trisubstituted 1; 3; 5-triazines; Pharmacology; Drug Discovery3003 Pharmaceutical Science; Organic Chemistrymedicine.symptomAntitumor activity
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Role of HSP60/HSP10 in Lung Cancer: Simple Biomarkers or Leading Actors?

2020

Cancers are one of the major challenges faced by modern medicine both because of their impact in terms of the amount of cases and of the ineffectiveness of therapies used today. A concrete support to the fight against them can be found in the analysis and understanding of the molecular mechanisms involving molecular chaperones. In particular, HSP60 and HSP10 seem to play an important role in carcinogenesis, supporting tumours in their proliferation, survival, and metastasis. Efforts must be directed toward finding ways to eliminate or block this “mistaken” chaperone. Therefore, the scientific community must develop therapeutic strategies that consider HSP60 and HSP10 as the possible target …

0301 basic medicineModern medicineDiseaseReview ArticleBioinformaticsmedicine.disease_causeMetastasis03 medical and health sciences0302 clinical medicinemedicineDiagnostic biomarkerLung cancerRC254-282biologybusiness.industrySettore BIO/16 - Anatomia UmanaNeoplasms. Tumors. Oncology. Including cancer and carcinogensHSP60 HSP10 LUNG CANCERmedicine.disease030104 developmental biologyOncology030220 oncology & carcinogenesisChaperone (protein)biology.proteinHSP60businessCarcinogenesis
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Identifying Prognostic SNPs in Clinical Cohorts: Complementing Univariate Analyses by Resampling and Multivariable Modeling

2016

Clinical cohorts with time-to-event endpoints are increasingly characterized by measurements of a number of single nucleotide polymorphisms that is by a magnitude larger than the number of measurements typically considered at the gene level. At the same time, the size of clinical cohorts often is still limited, calling for novel analysis strategies for identifying potentially prognostic SNPs that can help to better characterize disease processes. We propose such a strategy, drawing on univariate testing ideas from epidemiological case-controls studies on the one hand, and multivariable regression techniques as developed for gene expression data on the other hand. In particular, we focus on …

0301 basic medicineMultivariate analysisMicroarraysTest StatisticsGene Expressionlcsh:MedicineBioinformatics01 natural sciencesHematologic Cancers and Related DisordersCohort Studies010104 statistics & probabilityMathematical and Statistical TechniquesResamplingMedicine and Health Scienceslcsh:ScienceStatistical DataUnivariate analysisMultidisciplinarySimulation and ModelingMultivariable calculusRegression analysisHematologyMyeloid LeukemiaPrognosisRegressionBioassays and Physiological AnalysisOncologyResearch DesignPhysical SciencesStatistics (Mathematics)Research ArticleAcute Myeloid LeukemiaPermutationSingle-nucleotide polymorphismComputational biologyBiologyResearch and Analysis MethodsPolymorphism Single Nucleotide03 medical and health sciencesLeukemiasGeneticsHumansStatistical Methods0101 mathematicsDiscrete Mathematicslcsh:RUnivariateCancers and NeoplasmsBiology and Life SciencesModels Theoretical030104 developmental biologyCombinatoricsCase-Control StudiesMultivariate Analysislcsh:QMathematicsPLOS ONE
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The shared frameshift mutation landscape of microsatellite-unstable cancers suggests immunoediting during tumor evolution

2020

The immune system can recognize and attack cancer cells, especially those with a high load of mutation-induced neoantigens. Such neoantigens are abundant in DNA mismatch repair (MMR)-deficient, microsatellite-unstable (MSI) cancers. MMR deficiency leads to insertion/deletion (indel) mutations at coding microsatellites (cMS) and to neoantigen-inducing translational frameshifts. Here, we develop a tool to quantify frameshift mutations in MSI colorectal and endometrial cancer. Our results show that frameshift mutation frequency is negatively correlated to the predicted immunogenicity of the resulting peptides, suggesting counterselection of cell clones with highly immunogenic frameshift peptid…

0301 basic medicineMutation rateGeneral Physics and Astronomymedicine.disease_causeCOLORECTAL-CANCER0302 clinical medicineINDEL MutationMutation RateimmunologiaHLA AntigensNeoplasmsFrameshift Mutationlcsh:ScienceImmunologic SurveillanceGeneticsMutationMultidisciplinaryMISMATCH REPAIR DEFICIENCYQPEPTIDES3. Good healthkohdunrungon syöpäsyöpäsolutimmuunivaste030220 oncology & carcinogenesisTumour immunologyMicrosatellite InstabilityDNA mismatch repairINDEL MutationEXPRESSIONcongenital hereditary and neonatal diseases and abnormalitieskasvaimetDATABASESciencegastrointestinal cancerINSTABILITY3122 CancerssuolistosyövätBiologycomplex mixturesArticleGeneral Biochemistry Genetics and Molecular BiologyFrameshift mutationGastrointestinal cancer03 medical and health sciencesAntigens NeoplasmCOLONmedicineHumansCELLSelection GeneticIndelSIGNATUREStumour immunologyMicrosatellite instabilityGeneral ChemistryDNAmedicine.disease3126 Surgery anesthesiology intensive care radiologydigestive system diseases030104 developmental biologyImmunoeditinglcsh:Qmutaatiotbeta 2-MicroglobulinMicrosatellite Repeats
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One NF1 Mutation may Conceal Another

2019

Neurofibromatosis type 1 (NF1) is an autosomal dominant disease with complete penetrance but high variable expressivity. NF1 is caused by loss-of-function mutations in the NF1 gene, a negative regulator of the RAS-MAPK pathway. The NF1 gene has one of the highest mutation rates in human disorders, which may explain the outbreak of independent de novo variants in the same family. Here, we report the co-occurrence of pathogenic variants in the NF1 and SPRED1 genes in six families with NF1 and Legius syndrome, using next-generation sequencing. In five of these families, we observed the co-occurrence of two independent NF1 variants. All NF1 variants were classified as pathogenic, according to t…

0301 basic medicineMutation ratemedicine.medical_specialtySPRED1congenital hereditary and neonatal diseases and abnormalities<i>SPRED1</i>lcsh:QH426-470[SDV]Life Sciences [q-bio]030105 genetics & heredityBiologyneurofibromatosis type 103 medical and health sciencesGeneticsmedicineNeurofibromatosisneoplasmsGenetics (clinical)Legius syndromeGeneticsMolecular pathologyAutosomal dominant traitmedicine.diseasePenetrance<i>NF1</i>eye diseases3. Good healthnervous system diseases[SDV] Life Sciences [q-bio]Legius syndromelcsh:Genetics030104 developmental biologyNF1Medical geneticsSPRED1 Genede novo variantGenes
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Mesenchymal Transition of High-Grade Breast Carcinomas Depends on Extracellular Matrix Control of Myeloid Suppressor Cell Activity

2016

SummaryThe extracellular matrix (ECM) contributes to the biological and clinical heterogeneity of breast cancer, and different prognostic groups can be identified according to specific ECM signatures. In high-grade, but not low-grade, tumors, an ECM signature characterized by high SPARC expression (ECM3) identifies tumors with increased epithelial-to-mesenchymal transition (EMT), reduced treatment response, and poor prognosis. To better understand how this ECM3 signature is contributing to tumorigenesis, we expressed SPARC in isogenic cell lines and found that SPARC overexpression in tumor cells reduces their growth rate and induces EMT. SPARC expression also results in the formation of a h…

0301 basic medicineMyeloidMDSCGene Expressionmedicine.disease_causeT-Lymphocytes RegulatoryPolyethylene GlycolsExtracellular matrixMiceBreast cancerMyeloid CellsOsteonectinMast Cellslcsh:QH301-705.5Mice KnockoutAntigen PresentationMice Inbred BALB CEMTepithelial to mesenchymal transitionBreast cancer; COX-2; CXCL12; ECM; EMT; G-CSF; GM-CSF; MDSC; SPARC; aminobisphosphonates; cyclooxygenase-2; epithelial to mesenchymal transition; extracellular matrix; granulocyte colony-stimulating factor; granulocyte-macrophage colony-stimulating factor; myeloid-derived suppressor cellsCXCL12Granulocyte macrophage colony-stimulating factormedicine.anatomical_structurecyclooxygenase-2granulocyte-macrophage colony-stimulating factorFemalegranulocyte colony-stimulating factormedicine.drugEpithelial-Mesenchymal Transitionextracellular matrixAntineoplastic AgentsBreast NeoplasmsBiologySettore MED/08 - Anatomia PatologicaG-CSFGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesCell Line TumormedicineAnimalsHumansEpithelial–mesenchymal transitionECMMesenchymal stem cellSPARCGM-CSFCOX-2myeloid-derived suppressor cellsXenograft Model Antitumor AssaysIsogenic human disease modelsaminobisphosphonates030104 developmental biologylcsh:Biology (General)CelecoxibDoxorubicinImmunologyCancer researchMyeloid-derived Suppressor CellaminobisphosphonateNeoplasm GradingCarcinogenesisCell Reports
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Myeloid cells as orchestrators of the tumor microenvironment: novel targets for nanoparticular cancer therapy.

2016

Macrophages, myeloid-derived suppressor cells and tolerogenic dendritic cells are central players of a heterogeneous myeloid cell population, with the ability to suppress innate and adaptive immune responses and thus to promote tumor growth. Their influx and local proliferation are mainly induced by the cancers themselves, and their numbers in the tumor microenvironment and the peripheral blood correlate with decreased survival. Therapeutic targeting these innate immune cells, either aiming at their elimination or polarization toward tumor suppressive cells is an attractive novel approach to control tumor progression and block metastasis. We review the current understanding of cancer immun…

0301 basic medicineMyeloidPolymersmedicine.medical_treatmentPopulationBiomedical EngineeringMedicine (miscellaneous)BioengineeringDevelopmentBiology03 medical and health sciences0302 clinical medicineImmune systemNeoplasmsmedicineTumor MicroenvironmentAnimalsHumansGeneral Materials ScienceMyeloid CellsRNA Small InterferingeducationCancer immunologyeducation.field_of_studyTumor microenvironmentDrug CarriersInnate immune systemMacrophagesMyeloid-Derived Suppressor CellsImmunotherapyDendritic CellsImmunity Innate030104 developmental biologymedicine.anatomical_structureTumor progression030220 oncology & carcinogenesisImmunologyNanoparticlesImmunotherapyNanomedicine (London, England)
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Myeloid cell-synthesized coagulation Factor X dampens anti-tumor immunity

2019

Immune evasion in the tumor microenvironment (TME) is a crucial barrier for effective cancer therapy, and plasticity of innate immune cells may contribute to failures of targeted immunotherapies. Here, we show that rivaroxaban, a direct inhibitor of activated coagulation factor X (FX), promotes antitumor immunity by enhancing infiltration of dendritic cells and cytotoxic T cells at the tumor site. Profiling FX expression in the TME identifies monocytes and macrophages as crucial sources of extravascular FX. By generating mice with immune cells lacking the ability to produce FX, we show that myeloid cell-derived FX plays a pivotal role in promoting tumor immune evasion. In mouse models of ca…

0301 basic medicineMyeloidmedicine.medical_treatmentImmunologyCellMammary Neoplasms AnimalArticle03 medical and health sciencesMice0302 clinical medicineImmune systemmedicineCytotoxic T cellAnimalsHumansMyeloid CellsTumor microenvironmentInnate immune systembusiness.industryGeneral MedicineImmunotherapyMice Inbred C57BL030104 developmental biologymedicine.anatomical_structure030220 oncology & carcinogenesisFactor XCancer researchFemaleImmunotherapySignal transductionbusiness
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