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showing 10 items of 23890 documents

Persistent immune stimulation exacerbates genetically driven myeloproliferative disorders via stromal remodeling

2017

Abstract Systemic immune stimulation has been associated with increased risk of myeloid malignancies, but the pathogenic link is unknown. We demonstrate in animal models that experimental systemic immune activation alters the bone marrow stromal microenvironment, disarranging extracellular matrix (ECM) microarchitecture, with downregulation of secreted protein acidic and rich in cysteine (SPARC) and collagen-I and induction of complement activation. These changes were accompanied by a decrease in Treg frequency and by an increase in activated effector T cells. Under these conditions, hematopoietic precursors harboring nucleophosmin-1 (NPM1) mutation generated myeloid cells unfit for normal …

0301 basic medicineCancer ResearchStromal cellMyeloidMice TransgenicVascular RemodelingBiologyInbred C57BLTransgenicMice03 medical and health sciencesMyelogenousMyeloproliferative DisordersmedicineAnimalsHumansMyeloproliferative DisorderAnimals; Cell Proliferation; Humans; Mice; Mice Inbred C57BL; Mice Inbred CBA; Mice Transgenic; Myeloproliferative Disorders; Stromal Cells; Vascular Remodeling; Oncology; Cancer ResearchCell ProliferationMyeloproliferative DisordersAnimalStromal CellInbred CBANeutrophil extracellular trapsmedicine.diseaseMice Inbred C57BLHaematopoiesisLeukemia030104 developmental biologymedicine.anatomical_structureOncologyImmunologyMice Inbred CBABone marrowStromal CellsNucleophosminHuman
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Differential distribution and enrichment of non-coding RNAs in exosomes from normal and Cancer-associated fibroblasts in colorectal cancer.

2018

Exosome production from cancer-associated fibroblasts seems to be an important driver of tumor progression. We report the first in-depth biotype characterization of ncRNAs, analyzed by Next Generation Sequencing and Bioinformatics, expressed in established primary human normal and cancer-associated fibroblasts (CAFs) from cancer and normal mucosa tissues from 9 colorectal cancer patients, and/or packaged in their derived exosomes. Differential representation and enrichment analyses based on these ncRNAs revealed a significant number of differences between the ncRNA content of exosomes and the expression patterns of the normal and cancer-associated fibroblast cells. ncRNA regulatory elements…

0301 basic medicineCancer ResearchStromal cellRNA UntranslatedColorectal cancerBiologyExosomeslcsh:RC254-282Non-coding RNAs03 medical and health sciencesCancer-Associated FibroblastsCell MovementNext generation sequencingmedicineBiomarkers TumorHumansLiquid biopsyLetter to the EditorCells CulturedCell ProliferationTumor microenvironmentColon CancerLiquid biopsySequence Analysis RNACancerHigh-Throughput Nucleotide SequencingFibroblastsmedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPrognosisMicrovesiclesGene Expression Regulation Neoplastic030104 developmental biologyOncologyTumor microenvironmentTumor progressionCancer researchMolecular MedicineCancer-Associated FibroblastsColorectal Neoplasms
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Lack of a peroxiredoxin suppresses the lethality of cells devoid of electron donors by channelling electrons to oxidized ribonucleotide reductase

2017

The thioredoxin and glutaredoxin pathways are responsible of recycling several enzymes which undergo intramolecular disulfide bond formation as part of their catalytic cycles such as the peroxide scavengers peroxiredoxins or the enzyme ribonucleotide reductase (RNR). RNR, the rate-limiting enzyme of deoxyribonucleotide synthesis, is an essential enzyme relying on these electron flow cascades for recycling. RNR is tightly regulated in a cell cycle-dependent manner at different levels, but little is known about the participation of electron donors in such regulation. Here, we show that cytosolic thioredoxins Trx1 and Trx3 are the primary electron donors for RNR in fission yeast. Unexpectedly,…

0301 basic medicineCancer ResearchThioredoxin reductaseSynthesis PhaseYeast and Fungal ModelsBiochemistryElectron DonorsSchizosaccharomyces PombeThioredoxinsGlutaredoxinCell Cycle and Cell DivisionGenetics (clinical)Chemical ReactionsOxidesPeroxidesNucleic acidsChemistryRibonucleotide reductaseBiochemistryExperimental Organism SystemsCell ProcessesSchizosaccharomyces pombePhysical SciencesSynthesis phaseThioredoxinOxidation-ReductionResearch ArticleDNA Replicationlcsh:QH426-470DNA transcriptionElectron donorsBiologyDNA replicationResearch and Analysis MethodsCatalysisElectron Transport03 medical and health sciencesModel OrganismsSchizosaccharomycesRibonucleotide ReductasesOxidationGeneticsMolecular BiologyEcology Evolution Behavior and SystematicsGlutaredoxinsCell growthDNA replicationChemical CompoundsOrganismsFungiBiology and Life SciencesCell BiologyDNAPeroxiredoxinsbiology.organism_classificationYeastCell cycle and cell divisionCheckpoint Kinase 2lcsh:Genetics030104 developmental biologySchizosaccharomyces pombeGene expressionSchizosaccharomyces pombe ProteinsPeroxiredoxin
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Rationale for stimulator of interferon genes-targeted cancer immunotherapy

2017

International audience; The efficacy of checkpoint inhibitor therapy illustrates that cancer immunotherapy, which aims to foster the host immune response against cancer to achieve durable anticancer responses, can be successfully implemented in a routine clinical practice. However, a substantial proportion of patients does not benefit from this treatment, underscoring the need to identify alternative strategies to defeat cancer. Despite the demonstration in the 1990's that the detection of danger signals, including the nucleic acids DNA and RNA, by dendritic cells (DCs) in a cancer setting is essential for eliciting host defence, the molecular sensors responsible for recognising these dange…

0301 basic medicineCancer Research[SDV.IMM] Life Sciences [q-bio]/Immunologymedicine.medical_treatmentCancer immunotherapyBiologydanger signal03 medical and health sciencesImmune systemCancer immunotherapymedicine[ SDV.IMM ] Life Sciences [q-bio]/Immunologyinnate immunityInnate immune systemanticancer therapiesCancerImmunotherapyDNAadaptive immunityAcquired immune systemmedicine.diseaseeye diseases3. Good healthSting030104 developmental biologyOncologyStimulator of interferon genesImmunology[SDV.IMM]Life Sciences [q-bio]/ImmunologySTING
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Molecular Basis of Mismatch Repair Protein Deficiency in Tumors from Lynch Suspected Cases with Negative Germline Test Results

2020

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0301 basic medicineCancer Researchcongenital hereditary and neonatal diseases and abnormalitiesCARCINOMADNA mismatch repair3122 Cancerscolorectal cancersuolistosyövätBiologyGene mutationMLH1DIAGNOSISlcsh:RC254-282Article03 medical and health sciencesdeep sequencing0302 clinical medicineGermline mutationFREQUENT CAUSEMANAGEMENTLynchin oireyhtymäneoplasmspaksusuolisyöpäMUTATIONSPoint mutationMLH1METHYLATIONnutritional and metabolic diseasesNONPOLYPOSIS COLORECTAL-CANCERDEFECTSdiagnostiikkalcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensdigestive system diseases3. Good healthDNA-metylaatioMSH2MSH6030104 developmental biologyLynch syndromeOncologyMSH3syöpägeenitMSH2030220 oncology & carcinogenesisCancer researchDNA mismatch repairsyöpätauditCancers
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Pattern of Invasion in Human Pancreatic Cancer Organoids Is Associated with Loss of SMAD4 and Clinical Outcome

2020

Abstract Pancreatic ductal adenocarcinoma (PDAC) is an aggressive malignancy characterized by extensive local invasion and systemic spread. In this study, we employed a three-dimensional organoid model of human pancreatic cancer to characterize the molecular alterations critical for invasion. Time-lapse microscopy was used to observe invasion in organoids from 25 surgically resected human PDAC samples in collagen I. Subsequent lentiviral modification and small-molecule inhibitors were used to investigate the molecular programs underlying invasion in PDAC organoids. When cultured in collagen I, PDAC organoids exhibited two distinct, morphologically defined invasive phenotypes, mesenchymal an…

0301 basic medicineCancer Researchendocrine system diseasesPancreatic ductal adenocarcinoma (PDAC)RAC1CDC42AdenocarcinomaBiologyArticle03 medical and health sciences0302 clinical medicineHuman Pancreatic CancerCell MovementPancreatic cancerBiomarkers TumorTumor Cells CulturedmedicineOrganoidHumansNeoplasm InvasivenessCell ProliferationSmad4 ProteinRegulation of gene expressionCell growthMesenchymal stem cellPrognosismedicine.diseasePhenotypedigestive system diseasesGene Expression Regulation NeoplasticOrganoidsPancreatic NeoplasmsSurvival Rate030104 developmental biologyOncology030220 oncology & carcinogenesisembryonic structuresCancer researchCarcinoma Pancreatic DuctalSignal TransductionCancer Research
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Hereditary breast and ovarian cancer in families from southern Italy (Sicily)—Prevalence and geographic distribution of pathogenic variants in BRCA1/…

2020

Recent advances in the detection of germline pathogenic variants (PVs) in BRCA1/2 genes have allowed a deeper understanding of the BRCA-related cancer risk. Several studies showed a significant heterogeneity in the prevalence of PVs across different populations. Because little is known about this in the Sicilian population, our study was aimed at investigating the prevalence and geographic distribution of inherited BRCA1/2 PVs in families from this specific geographical area of Southern Italy. We retrospectively collected and analyzed all clinical information of 1346 hereditary breast and/or ovarian cancer patients genetically tested for germline BRCA1/2 PVs at University Hospital Policlini…

0301 basic medicineCancer Researchendocrine system diseasesPopulationSicilian populationBiologylcsh:RC254-282hereditary breast and ovarian cancerArticleGermlinefounder variantsgenetic testing03 medical and health sciences0302 clinical medicineBreast cancerbreast cancermedicineskin and connective tissue diseaseseducationGeneGenetic testinggermline pathogenic varianteducation.field_of_studyfounder variantmedicine.diagnostic_testGenetic heterogeneitylcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseBRCA1BRCA2language.human_language<i>BRCA1</i>030104 developmental biologyovarian cancerOncology030220 oncology & carcinogenesiscardiovascular systemlanguagegermline pathogenic variantsOvarian cancerSicilian<i>BRCA2</i>Demography
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The hallmarks of ovarian cancer: proliferation and cell growth

2020

Epithelial ovarian cancer (EOC) is a heterogeneous group of diseases with distinct biological and clinical behaviour. Despite the differences between them, the capability of tumour cells to continuously proliferate and avoid death is maintained among histotypes. This ability is the result of alterations at different levels, causing the deregulation of cell cycle and proliferative-related pathways. Even if the leading role is played by RB and TP53, changes in other molecular pathways are involved in the development of EOC. This ability can be exploited to generate in vitro and in vivo models resembling the conditions of tumour development in a patient. In vivo models, such as patient-derived…

0301 basic medicineCancer Researchendocrine system diseaseslcsh:MedicineBiologylcsh:RC254-282Article03 medical and health sciencesCell growth0302 clinical medicinemedicineEpithelial ovarian cancerCell proliferationHeterogeneous groupCell growthlcsh:RCell cycleEpithelial ovarian cancerlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseAnimal models030104 developmental biologyOncologyTumour development030220 oncology & carcinogenesisGenetically Engineered MouseCancer researchOvarian cancerEJC Supplements
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Urinary Metabolic Signatures Detect Recurrences in Non-Muscle Invasive Bladder Cancer

2019

Patients with non-muscle invasive bladder cancer (NMIBC) undergo lifelong monitoring based on repeated cystoscopy and urinary cytology due to the high recurrence rate of this tumor. Nevertheless, these techniques have some drawbacks, namely, low accuracy in detection of low-grade tumors, omission of pre-neoplastic lesions and carcinomas in situ (CIS), invasiveness, and high costs. This work aims to identify a urinary metabolomic signature of recurrence by proton Nuclear Magnetic Resonance (1H NMR) spectroscopy for the follow-up of NMIBC patients. To do this, changes in the urinary metabolome before and after transurethral resection (TUR) of tumors are analyzed and a Partial Least Square Dis…

0301 basic medicineCancer Researchmedicine.medical_specialtyUrinary systemmetaboliteUrologylcsh:RC254-282Article03 medical and health sciences0302 clinical medicineMetabolomicsCytologyMetabolomeMedicineUrologiametabolic pathwaysCàncerBladder cancermedicine.diagnostic_testbusiness.industryrecurrence predictionCystoscopymedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmetabolomicsnuclear magnetic resonance030104 developmental biologyOncology030220 oncology & carcinogenesisBiomarker (medicine)bladder cancerbiomarkerbusinessNon muscle invasivebiomarker bladder cancer metabolic pathways metabolite metabolomics nuclear magnetic resonance recurrence predictionCancers
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A common SNP in the UNG gene decreases ovarian cancer risk in BRCA2 mutation carriers

2018

Single nucleotide polymorphisms (SNPs) in DNA glycosylase genes involved in the base excision repair (BER) pathway can modify breast and ovarian cancer risk in BRCA1 and BRCA2 mutation carriers. We previously found that SNP rs34259 in the uracil-DNA glycosylase gene (UNG) might decrease ovarian cancer risk in BRCA2 mutation carriers. In the present study, we validated this finding in a larger series of familial breast and ovarian cancer patients to gain insights into how this UNG variant exerts its protective effect. We found that rs34259 is associated with significant UNG downregulation and with lower levels of DNA damage at telomeres. In addition, we found that this SNP is associated with…

0301 basic medicineCancer Researchmedicine.medical_specialtyendocrine system diseasesUracil-DNA glycosylaseEuropean Regional Development Fundlcsh:RC254-282Polymorphism Single Nucleotide03 medical and health sciences0302 clinical medicineBRCA2 MutationRisk FactorsPolitical scienceHealthy volunteersGeneticsmedicineHumansSNPGenetic Predisposition to DiseaseUracil-DNA Glycosidaseskin and connective tissue diseasesResearch ArticlesBRCA2 ProteinOvarian NeoplasmsNetwork onOxidative stress susceptibilityGeneral MedicineMiddle Agedlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseBRCA2female genital diseases and pregnancy complicationsuracil‐DNA glycosylase030104 developmental biologyCancer risk modifierOncology030220 oncology & carcinogenesisFamily medicineMutationMolecular MedicineDNA damageFemaleChristian ministryTelomere damageOvarian cancerHuman cancerResearch Article
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