Search results for "anatomia patologica"

showing 10 items of 240 documents

Longevity: Lesson from model organisms

2019

Research on longevity and healthy aging promises to increase our lifespan and decrease the burden of degenerative diseases with important social and economic effects. Many aging theories have been proposed, and important aging pathways have been discovered. Model organisms have had a crucial role in this process because of their short lifespan, cheap maintenance, and manipulation possibilities. Yeasts, worms, fruit flies, or mammalian models such as mice, monkeys, and recently, dogs, have helped shed light on aging processes. Genes and molecular mechanisms that were found to be critical in simple eukaryotic cells and species have been confirmed in humans mainly by the functional analysis of…

0301 basic medicineAginglcsh:QH426-470Settore MED/06 - Oncologia Medicamedia_common.quotation_subjectved/biology.organism_classification_rank.speciesLongevityReviewBiologySignal transductionSettore MED/08 - Anatomia PatologicaModels Biologicalmodel systems03 medical and health sciences0302 clinical medicineModel systemYeastsGeneticsAnimalsHumansHealthy agingSettore MED/49 - Scienze Tecniche Dietetiche ApplicateModel organismGeneGenetics (clinical)Cellular Senescencemedia_commonMammalsved/biologyLongevityEukaryotalcsh:GeneticsSettore MED/18 - Chirurgia Generale030104 developmental biologyEvolutionary biologyHuman longevityModels AnimalDrosophilaMolecular senescence030217 neurology & neurosurgeryBiomarkers
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Virus-encoded microRNA contributes to the molecular profile of EBV-positive Burkitt lymphomas

2015

Burkitt lymphoma (BL) is an aggressive neoplasm characterized by consistent morphology and phenotype, typical clinical behavior and distinctive molecular profile. The latter is mostly driven by the MYC over-expression associated with the characteristic translocation (8;14) (q24; q32) or with variant lesions. Additional genetic events can contribute to Burkitt Lymphoma pathobiology and retain clinical significance. A pathogenetic role for Epstein-Barr virus infection in Burkitt lymphomagenesis has been suggested; however, the exact function of the virus is largely unknown. In this study, we investigated the molecular profiles (genes and microRNAs) of Epstein-Barr virus-positive and -negative…

0301 basic medicineBART6; Burkitt lymphoma; EBV; miRNA; pathogenesisEpstein-Barr Virus InfectionsHerpesvirus 4 HumanpathogenesiRNA-binding proteinRNA-Binding ProteinEpstein-Barr Virus Infectionhemic and lymphatic diseasesCluster AnalysisViralOligonucleotide Array Sequence AnalysisGeneticsBART6; Burkitt lymphoma; EBV; miRNA; pathogenesis; Burkitt Lymphoma; Cluster Analysis; Cytoskeletal Proteins; Epstein-Barr Virus Infections; Gene Expression Profiling; Gene Expression Regulation Neoplastic; Gene Expression Regulation Viral; Herpesvirus 4 Human; Host-Pathogen Interactions; Humans; Immunohistochemistry; MicroRNAs; Neoplasm Proteins; Oligonucleotide Array Sequence Analysis; Phospholipase C delta; RNA Viral; RNA-Binding Proteins; Reverse Transcriptase Polymerase Chain Reaction; ras Proteins; OncologyReverse Transcriptase Polymerase Chain ReactionpathogenesisMicrofilament ProteinsIntracellular Signaling Peptides and ProteinsBurkitt lymphomaRNA-Binding ProteinsMicroRNAPhenotypeImmunohistochemistryNeoplasm ProteinsHost-Pathogen InteractionGene Expression Regulation NeoplasticOncologyHost-Pathogen InteractionsRNA ViralHumanResearch PaperGene Expression Regulation ViralBART6BiologySettore MED/08 - Anatomia PatologicaVirusNeoplasm Protein03 medical and health sciencesEBVmicroRNACytoskeletal ProteinmedicineHumansEpstein–Barr virus infectionGenemiRNANeoplasticCluster AnalysiOligonucleotide Array Sequence AnalysiGene Expression ProfilingHerpesvirus 4ras Proteinmedicine.diseaseLymphomaGene expression profilingCytoskeletal ProteinsMicroRNAs030104 developmental biologyGene Expression Regulationras ProteinsRNABART6; EBV; burkitt lymphoma; miRNA; pathogenesisPhospholipase C deltaOncotarget
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Mutant p53 induces Golgi tubulo-vesiculation driving a prometastatic secretome

2020

TP53 missense mutations leading to the expression of mutant p53 oncoproteins are frequent driver events during tumorigenesis. p53 mutants promote tumor growth, metastasis and chemoresistance by affecting fundamental cellular pathways and functions. Here, we demonstrate that p53 mutants modify structure and function of the Golgi apparatus, culminating in the increased release of a pro-malignant secretome by tumor cells and primary fibroblasts from patients with Li-Fraumeni cancer predisposition syndrome. Mechanistically, interacting with the hypoxia responsive factor HIF1α, mutant p53 induces the expression of miR-30d, which in turn causes tubulo-vesiculation of the Golgi apparatus, leading …

0301 basic medicineBiopsyGeneral Physics and AstronomyGolgi ApparatusAnimals Biopsy Breast Neoplasms Cell Line Tumor Cell Transformation Neoplastic Female Fibroblasts Gene Expression Regulation Neoplastic Golgi Apparatus Humans Hypoxia-Inducible Factor 1 alpha Subunit Li-Fraumeni Syndrome Mice MicroRNAs Microtubules Mutation Primary Cell Culture Secretory Vesicles Signal TransductionSkin Tumor Microenvironment Tumor Suppressor Protein p53 Xenograft Model Antitumor Assays02 engineering and technologymedicine.disease_causeCell TransformationMicrotubulesSettore BIO/09 - FisiologiaMetastasisLi-Fraumeni SyndromeMiceTumor MicroenvironmentGolgisecretory machinerySuper-resolution microscopyAnimals; Biopsy; Breast Neoplasms; Cell Line Tumor; Cell Transformation Neoplastic; Female; Fibroblasts; Gene Expression Regulation Neoplastic; Golgi Apparatus; Humans; Hypoxia-Inducible Factor 1 alpha Subunit; Li-Fraumeni Syndrome; Mice; MicroRNAs; Microtubules; Mutation; Primary Cell Culture; Secretory Vesicles; Signal Transduction; Skin; Tumor Microenvironment; Tumor Suppressor Protein p53; Xenograft Model Antitumor Assayslcsh:ScienceSkinMultidisciplinaryTumorChemistrymutant p53QCell migrationMicroRNASecretomics021001 nanoscience & nanotechnologyCell biologyGene Expression Regulation NeoplasticCell Transformation NeoplasticsymbolsFibroblastmiR-30dFemaleHypoxia-Inducible Factor 10210 nano-technologyBreast NeoplasmHumanSignal TransductionCancer microenvironmentStromal cellSecretory VesicleSciencePrimary Cell CultureBreast NeoplasmsMicrotubuleGolgi ApparatuSettore MED/08 - Anatomia Patologicaalpha SubunitGeneral Biochemistry Genetics and Molecular BiologyArticleCell Line03 medical and health sciencessymbols.namesakeCell Line TumormedicineAnimalsHumansSettore MED/05 - Patologia ClinicaSecretionTumor microenvironmentNeoplasticAnimalSecretory VesiclesGeneral ChemistryOncogenesGolgi apparatusHDAC6FibroblastsMicroreviewHypoxia-Inducible Factor 1 alpha SubunitmicroenvironmentXenograft Model Antitumor AssaysMicroRNAs030104 developmental biologyGene Expression RegulationMutationlcsh:QTumor Suppressor Protein p53Carcinogenesis
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Gut Microbiota Condition the Therapeutic Efficacy of Trastuzumab in HER2-Positive Breast Cancer.

2021

Abstract Emerging evidence indicates that gut microbiota affect the response to anticancer therapies by modulating the host immune system. In this study, we investigated the impact of gut microbiota on immune-mediated trastuzumab antitumor efficacy in preclinical models of HER2-positive breast cancer and in 24 patients with primary HER2-positive breast cancer undergoing trastuzumab-containing neoadjuvant treatment. In mice, the antitumor activity of trastuzumab was impaired by antibiotic administration or fecal microbiota transplantation from antibiotic-treated donors. Modulation of the intestinal microbiota was reflected in tumors by impaired recruitment of CD4+ T cells and granzyme B–posi…

0301 basic medicineCD4-Positive T-LymphocytesCancer ResearchReceptor ErbB-2medicine.medical_treatmentGut floraGranzymesMice0302 clinical medicineAntineoplastic Agents ImmunologicalTrastuzumabTumor Microenvironmentskin and connective tissue diseasesNeoadjuvant therapybiologyFecal Microbiota TransplantationInterleukin-12Neoadjuvant TherapyAnti-Bacterial AgentsTreatment OutcomeOncology030220 oncology & carcinogenesisStreptomycinCytokinesGut microbiota trastuzumab breast cancerFemaleTaxoidsmedicine.drugBridged-Ring CompoundsBreast NeoplasmsSettore MED/08 - Anatomia PatologicaNitric Oxide03 medical and health sciencesImmune systemBreast cancerVancomycinmedicineAnimalsHumansCyclophosphamideImmunity Mucosalbusiness.industryLachnospiraceaeDendritic cellDendritic CellsTrastuzumabbiology.organism_classificationmedicine.diseaseGastrointestinal Microbiome030104 developmental biologyGranzymeDoxorubicinImmune Systembiology.proteinCancer researchInterferonsbusinessCancer research
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Tumor-Derived Prostaglandin E2 Promotes p50 NF-κB-Dependent Differentiation of Monocytic MDSCs

2020

Abstract Myeloid-derived suppressor cells (MDSC) include immature monocytic (M-MDSC) and granulocytic (PMN-MDSC) cells that share the ability to suppress adaptive immunity and to hinder the effectiveness of anticancer treatments. Of note, in response to IFNγ, M-MDSCs release the tumor-promoting and immunosuppressive molecule nitric oxide (NO), whereas macrophages largely express antitumor properties. Investigating these opposing activities, we found that tumor-derived prostaglandin E2 (PGE2) induces nuclear accumulation of p50 NF-κB in M-MDSCs, diverting their response to IFNγ toward NO-mediated immunosuppression and reducing TNFα expression. At the genome level, p50 NF-κB promoted binding …

0301 basic medicineCancer ResearchCellular differentiationProstaglandin E2 receptormedicine.medical_treatmentMelanoma ExperimentalApoptosisSettore MED/08 - Anatomia PatologicaNitric OxideDinoprostoneMonocytesInterferon-gammaMice03 medical and health sciences0302 clinical medicineImmune systemOxytocicsImmune ToleranceTumor Cells CulturedmedicineAnimalsHumansProstaglandin E2Cell ProliferationChemistryMyeloid-Derived Suppressor CellsNF-kappa B p50 SubunitCell DifferentiationImmunotherapyAcquired immune systemPancreatic Neoplasms030104 developmental biologyOncologyp50 NF-κB differentiation of monocytic MDSC.030220 oncology & carcinogenesisMyeloid-derived Suppressor CellCancer researchTumor necrosis factor alphaColorectal Neoplasmsmedicine.drugCancer Research
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AP2α controls the dynamic balance between miR-126&126* and miR-221&222 during melanoma progression

2016

Accumulating evidences have shown the association between aberrantly expressed microRNAs (miRs) and cancer, where these small regulatory RNAs appear to dictate the cell fate by regulating all the main biological processes. We demonstrated the responsibility of the circuitry connecting the oncomiR-221&222 with the tumor suppressors miR-126&126∗ in melanoma development and progression. According to the inverse correlation between endogenous miR-221&222 and miR-126&126∗, respectively increasing or decreasing with malignancy, their enforced expression or silencing was sufficient for a reciprocal regulation. In line with the opposite roles of these miRs, protein analyses confirmed the reverse ex…

0301 basic medicineCancer ResearchCellular differentiationSettore MED/08 - Anatomia Patologicagrowth-factorCell fate determinationBiologyFatty Acid-Binding ProteinsBioinformaticsap-2 transcription factorlaw.inventioncutaneous melanoma03 medical and health sciencesMolecular Biology; Cancer Research; Genetics0302 clinical medicinelawTranscription (biology)Cell Line TumormicroRNAGeneticsmedicineHumansGene silencingMelanomaMolecular BiologyPsychological repressionsquamous-cell carcinoma; ap-2 transcription factor; cutaneous melanoma; growth-factor; metastatic melanoma; terminal fragment; cancer-cells; tumor-growth; mir-126; methylationMelanomaCell Differentiationsquamous-cell carcinomatumor-growthmedicine.diseaseMicroRNAscancer-cells030104 developmental biologyterminal fragmentmir-126030220 oncology & carcinogenesisDisease ProgressionCancer researchSuppressorOriginal Articlemethylationmetastatic melanomaOncogene
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Breast Cancer Organoids Model Patient-Specific Response to Drug Treatment

2020

Tumor organoids are tridimensional cell culture systems that are generated in vitro from surgically resected patients&rsquo

0301 basic medicineCancer ResearchMechanotransductionBreast cancer; Dasatinib; Drug testing; Heterogeneity; Mechanotransduction; Patient‐derived tumor organoids; Statin; YAPPatient‐derived tumor organoidCellDasatinibDrug resistanceSettore MED/08 - Anatomia PatologicaBiologylcsh:RC254-282Article03 medical and health sciencesBreast cancer0302 clinical medicineBreast cancerbreast cancermedicineOrganoidSettore MED/05 - Patologia Clinicadasatinibdrug testingmechanotransductionpatient-derived tumor organoidsGenetic heterogeneitystatinStatinDrug testingBreast cancerDasatinib Drug testing Drug testing Heterogeneity Patient‐derived tumor organoids Statin YAPmedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensIn vitroDasatinib030104 developmental biologymedicine.anatomical_structureOncologyCell culture030220 oncology & carcinogenesisCancer researchPatient‐derived tumor organoidsYAPHeterogeneityheterogeneitymedicine.drugCancers
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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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Mast cells crosstalk with B cells in the gut and sustain IgA response in the inflamed intestine.

2021

B lymphocytes are among the cell types whose effector functions are modulated by mast cells (MCs). The B/MC crosstalk emerged in several pathological settings, notably the colon of inflammatory bowel disease (IBD) patients is a privileged site in which MCs and IgA+ cells physically interact. Herein, by inducing conditional depletion of MCs in red MC and basophil (RMB) mice, we show that MCs control B cell distribution in the gut and IgA serum levels. Moreover, in dextran sulfate sodium (DSS)-treated RMB mice, the presence of MCs is fundamental for the enlargement of the IgA+ population in the bowel and the increase of systemic IgA production. Since both conventional B-2 and peritoneal-deriv…

0301 basic medicineCell typeColon[SDV]Life Sciences [q-bio]ImmunologyPopulationInflammationBasophilBiologySettore MED/08 - Anatomia Patologicabehavioral disciplines and activitiesInflammatory bowel diseasecell-to-cell interplay colitis IgAinnate-like B cells mast cells03 medical and health sciencesMice0302 clinical medicinemedicineImmunology and AllergyAnimalsMast CellsColitisIntestinal MucosaeducationB cellComputingMilieux_MISCELLANEOUSInflammationeducation.field_of_studyB-LymphocytesTumor Necrosis Factor-alphaDextran Sulfatemedicine.diseaseColitisInflammatory Bowel DiseaseshumanitiesInnate-like B cellsGastrointestinal MicrobiomeImmunoglobulin AMice Inbred C57BLCrosstalk (biology)030104 developmental biologymedicine.anatomical_structureCell-to-cell interplayCell-to-cell interplay; Colitis; IgA; Innate-like B cells; Mast cellsImmunologymedicine.symptomIgA030215 immunologyEuropean journal of immunologyReferences
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ATR expands embryonic stem cell fate potential in response to replication stress

2020

Fondazione Italiana per la Ricerca sul Cancro FIRC 18112 Sina Atashpaz.Fondazione Umberto Veronesi Sina Atashpaz Associazione Italiana per la Ricerca sul Cancro AIRC 5xmille METAMECH program Vincenzo Costanzo Giovanni Armenise-Harvard Foundation Vincenzo Costanzo European Research Council Consolidator grant 614541 Vincenzo Costanzo Associazione Italiana per la Ricerca sul Cancro Fellowship 23961 Negar ArghavanifarDanish Cancer Society KBVU-2014 Andres Joaquin Lopez-Contreras Danish Council for Independent Research Sapere Aude, DFF Starting Grant 2014 Andres Joaquin Lopez-Contreras European Research Council ERC-2015-STG-679068 Andres Joaquin Lopez-Contreras Danish National Research Foundatio…

0301 basic medicineEndogenyAtaxia Telangiectasia Mutated ProteinsMice0302 clinical medicineTandem Mass SpectrometryTranscription (biology)GENE ATRcell biologyCloning MolecularBiology (General)Cells Cultured0303 health sciencesGeneral NeuroscienceQRTotipotentCell DifferentiationEmbryoGeneral MedicineCell biologyMedicinebiological phenomena cell phenomena and immunityResearch ArticleQH301-705.5replication stressDNA damageScienceSettore MED/08 - Anatomia PatologicaBiologyGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesAnimalsRNA MessengerGeneEmbryonic Stem CellsmouseCell Proliferation030304 developmental biologyMessenger RNAGeneral Immunology and MicrobiologyChimeraSequence Analysis RNAEmbryogenesisTELOMERE ELONGATIONEPIGENETIC RESTRICTIONembryonic stem cellEmbryonic stem cellATR030104 developmental biologyGene Expression RegulationDNA-DAMAGECheckpoint Kinase 1GENOMIC STABILITY030217 neurology & neurosurgeryChromatography LiquidDNA DamageeLife
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