Search results for "OSiS"

showing 10 items of 15931 documents

Lack of association between screening interval and cancer stage in Lynch syndrome may be accounted for by over-diagnosis; a prospective Lynch syndrom…

2019

Background Recent epidemiological evidence shows that colorectal cancer (CRC) continues to occur in carriers of pathogenic mismatch repair (path_MMR) variants despite frequent colonoscopy surveillance in expert centres. This observation conflicts with the paradigm that removal of all visible polyps should prevent the vast majority of CRC in path_MMR carriers, provided the screening interval is sufficiently short and colonoscopic practice is optimal. Methods To inform the debate, we examined, in the Prospective Lynch Syndrome Database (PLSD), whether the time since last colonoscopy was associated with the pathological stage at which CRC was diagnosed during prospective surveillance. Path_MMR…

0301 basic medicineCOLONOSCOPIC SURVEILLANCEColorectal cancerColonoscopy030105 genetics & hereditycomputer.software_genreFAMILIESCOLORECTAL-CANCERBreast cancer screening0302 clinical medicine610 Medical sciences MedicineEpidemiologytähystysStage (cooking)Hereditary nonpolyposis colorectal cancerMUTATIONGenetics (clinical)RISKSurveillanceDatabasemedicine.diagnostic_testIncidence (epidemiology)Colonoscopylcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensLynch syndrome3. Good healthOncology030220 oncology & carcinogenesisendoskopiaScreeningsyöpätauditkoloskopiamedicine.medical_specialtylcsh:QH426-4703122 Cancers610suolistosyövätmikrosatelliititlcsh:RC254-282Mismatch repair03 medical and health sciencesCàncer colorectalmedicineEndoscòpiaLynchin oireyhtymäperinnölliset tauditseulontatutkimusbusiness.industryResearchColonoscòpiaMicrosatellite instabilityEndoscopyDNAdiagnostiikkamedicine.diseaseColorectal cancerdigestive system diseasesHereditary cancerADENOMAlcsh:GeneticsLynch syndromeOver-diagnosisMicrosatellite instabilitytarkkailubusinesscomputer
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Colorectal Carcinogenesis: Role of Oxidative Stress and Antioxidants

2017

One of the contributory causes of colon cancer is the negative effect of reactive oxygen species on DNA repair mechanisms. Currently, there is a growing support for the concept that oxidative stress may be an important etiological factor for carcinogenesis. The purpose of this review is to elucidate the role of oxidative stress in promoting colorectal carcinogenesis and to highlight the potential protective role of antioxidants. Several studies have documented the importance of antioxidants in countering oxidative stress and preventing colorectal carcinogenesis. However, there are conflicting data in the literature concerning its proper use in humans, since these studies did not yield defin…

0301 basic medicineCancer ResearchCarcinogenesisSettore MED/06 - Oncologia MedicaColorectal cancerDNA repairCellReviewColorectal Neoplasmmedicine.disease_causeAntioxidants03 medical and health sciences0302 clinical medicineAntioxidants; Colorectal cancer; Dysbiosis; Oxidative stress; Review; Animals; Antioxidants; Carcinogenesis; Colorectal Neoplasms; Humans; Reactive Oxygen Species; Oxidative Stress; Oncology; Cancer ResearchAnimalsHumansMedicinecolorectal cancer dysbiosis microbioma oxodative stress carcinogenesiCarcinogenesichemistry.chemical_classificationReactive oxygen speciesAnimalbusiness.industryOxidative StreGeneral MedicineColorectal carcinogenesismedicine.diseaseColorectal cancerDysbiosiOxidative StressSettore MED/18 - Chirurgia Generalecolorectal cancer dysbiosis microbioma oxodative stress carcinogenesis030104 developmental biologymedicine.anatomical_structureOncologyBiochemistrychemistry030220 oncology & carcinogenesisCancer researchAntioxidantColorectal NeoplasmsReactive Oxygen SpeciesReactive Oxygen SpeciebusinessCarcinogenesisDysbiosisOxidative stressHumanAnticancer Research
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Oleocanthal exerts antitumor effects on human liver and colon cancer cells through ROS generation

2017

The beneficial health properties of the Mediterranean diet are well recognized. The principle source of fat in Mediterranean diet is extra-virgin olive oil (EVOO). Oleocanthal (OC) is a naturally occurring minor phenolic compound isolated from EVOO, which has shown a potent anti-inflammatory activity, by means of its ability to inhibit the cyclooxygenase (COX) enzymes COX-1 and COX-2. A large body of evidence indicates that phenols exhibit anticancer activities. The aim of the present study was to evaluate the potential anticancer effects of OC in hepatocellular carcinoma (HCC) and colorectal carcinoma (CRC) models. A panel of human HCC (HepG2, Huh7, Hep3B and PLC/PRF/5) and CRC (HT29, SW48…

0301 basic medicineCancer ResearchCarcinoma HepatocellularHepatocellular carcinomaOleocanthalExtra-virgin olive oilCellApoptosisCyclopentane Monoterpenes03 medical and health scienceschemistry.chemical_compound0302 clinical medicinePhenolsOleocanthalmedicineHumansCyclooxygenase InhibitorsViability assayOlive OilCaspaseCell ProliferationAldehydesbiologyCell growthLiver NeoplasmsApoptosiHep G2 CellsCell cycledigestive system diseasesColorectal carcinoma030104 developmental biologymedicine.anatomical_structureOncologychemistryApoptosisCell culture030220 oncology & carcinogenesisImmunologybiology.proteinCancer researchReactive oxygen specieColorectal NeoplasmsReactive Oxygen SpeciesDNA DamageInternational Journal of Oncology
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Disruption of TCF/β-Catenin Binding Impairs Wnt Signaling and Induces Apoptosis in Soft Tissue Sarcoma Cells

2017

Abstract Soft tissue sarcomas (STS) are malignant tumors of mesenchymal origin and represent around 1% of adult cancers, being a very heterogeneous group of tumors with more than 50 different subtypes. The Wnt signaling pathway is involved in the development and in the regulation, self-renewal, and differentiation of mesenchymal stem cells, and plays a role in sarcomagenesis. In this study, we have tested pharmacologic inhibition of Wnt signaling mediated by disruption of TCF/β-catenin binding and AXIN stabilization, being the first strategy more efficient in reducing cell viability and downstream effects. We have shown that disruption of TCF/β-catenin binding with PKF118-310 produces in vi…

0301 basic medicineCancer ResearchCell SurvivalAntineoplastic AgentsApoptosisPyrimidinonesBiology03 medical and health sciences0302 clinical medicineCell Line TumormedicineHumansDoxorubicinViability assayWnt Signaling Pathwaybeta CateninCell ProliferationTriazinesCell growthCell CycleMesenchymal stem cellWnt signaling pathwayDrug SynergismSarcomaCell cycleMolecular biology030104 developmental biologyOncologyDoxorubicinCell culture030220 oncology & carcinogenesisCateninCancer researchTCF Transcription FactorsProtein Bindingmedicine.drugMolecular Cancer Therapeutics
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Trabectedin triggers direct and NK-mediated cytotoxicity in multiple myeloma

2019

Background Genomic instability is a feature of multiple myeloma (MM), and impairment in DNA damaging response (DDR) has an established role in disease pathobiology. Indeed, a deregulation of DNA repair pathways may contribute to genomic instability, to the establishment of drug resistance to genotoxic agents, and to the escape from immune surveillance. On these bases, we evaluated the role of different DDR pathways in MM and investigated, for the first time, the direct and immune-mediated anti-MM activity of the nucleotide excision repair (NER)-dependent agent trabectedin. Methods Gene-expression profiling (GEP) was carried out with HTA2.0 Affymetrix array. Evaluation of apoptosis, cell cyc…

0301 basic medicineCancer ResearchCell cycle checkpointNatural killerDNA repairmedicine.medical_treatmentMyelomalcsh:RC254-28203 medical and health sciences0302 clinical medicineMicro-RNAmedicineHumansMolecular BiologyAntineoplastic Agents AlkylatingTrabectedin3D-modelChemistrylcsh:RC633-647.5ResearchMicro-RNAsHematologylcsh:Diseases of the blood and blood-forming organsCell cycleNKG2Dlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensKiller Cells Natural030104 developmental biologyCytokineOncologyApoptosis3D-models030220 oncology & carcinogenesis3D-models; Micro-RNAs; Myeloma; Natural killer; TrabectedinCancer researchDNA fragmentationMultiple Myelomamedicine.drugTrabectedinJournal of Hematology & Oncology
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Molecular, Biological and Structural Features of VL CDR-1 Rb44 Peptide, Which Targets the Microtubule Network in Melanoma Cells

2019

Microtubules are important drug targets in tumor cells, owing to their role in supporting and determining the cell shape, organelle movement and cell division. The complementarity-determining regions (CDRs) of immunoglobulins have been reported to be a source of anti-tumor peptide sequences, independently of the original antibody specificity for a given antigen. We found that, the anti-Lewis B mAb light-chain CDR1 synthetic peptide Rb44, interacted with microtubules and induced depolymerization, with subsequent degradation of actin filaments, leading to depolarization of mitochondrial membrane-potential, increase of ROS, cell cycle arrest at G2/M, cleavage of caspase-9, caspase-3 and PARP, …

0301 basic medicineCancer ResearchCell divisionComplementarity determining regionCleavage (embryo)lcsh:RC254-28203 medical and health sciences0302 clinical medicineDownregulation and upregulationMicrotubulecomplementarity-determining regionActinbiologyChemistryIntrinsic apoptosisapoptosislcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogenspeptideCell biology030104 developmental biologyTubulintubulinOncology030220 oncology & carcinogenesisbiology.proteinmetastatic melanomamicrotubuleFrontiers in Oncology
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Intraspinal stem cell transplantation for amyotrophic lateral sclerosis: Ready for efficacy clinical trials?

2016

Intraspinal stem cell (SC) transplantation represents a new therapeutic approach for amyotrophic lateral sclerosis (ALS) clinical trials. There are considerable difficulties in designing future efficacy trials, some related to the field of ALS and some that are specific to SCs or the mode of delivery. In October 2015, the most controversial points on SC transplantation were addressed during an international workshop intended to bring together international SC and ALS researchers in a public discussion on a topic for which expertise is limited. During the meeting, a discussion was started on the basic structure of the ideal clinical trial testing the efficacy and safety of SC transplantation…

0301 basic medicineCancer ResearchCell- and Tissue-Based Therapy0302 clinical medicinePublic discussionNeural Stem CellsImmunology and AllergyNeural Stem CellALS; clinical trials; stem cells; transplantation; Immunology and Allergy; Immunology; Oncology; Genetics (clinical); Cell Biology; Cancer Research; TransplantationAmyotrophic lateral sclerosisGenetics (clinical)clinical trialMiddle AgedOncologyStem cellSafetyHumanAdultmedicine.medical_specialtyConsensusAdolescentImmunologyConsensu03 medical and health sciencesTherapeutic approachYoung AdultClinical Trials Phase II as Topicstem cellsmedicineHumansIntensive care medicineAgedclinical trialsTransplantationbusiness.industryAmyotrophic Lateral SclerosisBIO/13 - BIOLOGIA APPLICATACell Biologymedicine.diseasestem cellClinical trialTransplantation030104 developmental biologyClinical Trials Phase III as TopicImmunologyALSbusiness030217 neurology & neurosurgeryAmyotrophic Lateral SclerosiStem Cell TransplantationCytotherapy
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Extracellular Vesicles Shed by Melanoma Cells Contain a Modified Form of H1.0 Linker Histone and H1.0 mRNA-binding Proteins

2016

Extracellular vesicles (EVs) are shed in the extracellular environment by both prokaryotes and eukaryotes. Although produced from both normal and cancer cells, malignant cells release a much higher amount of EVs, which also contain tumor-specific proteins and RNAs. We previously found that G26/24 oligodendroglioma cells shed EVs that contain the pro-apoptotic factors FasL and TRAIL1-2. Interestingly, G26/24 release, via EVs, extracellular matrix remodelling proteases3, and H1° histone protein4, and mRNA. To shed further light on the role of EVs in discarding proteins and mRNAs otherwise able to counteract proliferative signals, we studied a melanoma cell line (A375). We found that also thes…

0301 basic medicineCancer ResearchCellular differentiationBlotting WesternFluorescent Antibody TechniqueMYEF2ApoptosisRNA-binding proteinexosomesmembrane vesiclesReal-Time Polymerase Chain ReactionChromatography AffinityHistones03 medical and health sciencesH1.0 linker histone; RNA-binding proteins (RBPs); extracellular vesicles (EVs) membrane vesicles (MVs); exosomes; MYEF2Settore BIO/10 - BiochimicaTumor Cells CulturedHumansexosomeSecretionRNA MessengerSettore BIO/06 - Anatomia Comparata E Citologiamelanoma cell line (A375) myelin expression factor-2 (MYEF2)MelanomaTranscription factorCell ProliferationH1.0 linker histonebiologyReverse Transcriptase Polymerase Chain ReactionEXTRACELLULAR VESICLESRNA-Binding ProteinsRNACell DifferentiationArticlesCell biologyBlotCell Transformation Neoplastic030104 developmental biologyHistoneOncologySpectrometry Mass Matrix-Assisted Laser Desorption-IonizationCancer cellbiology.proteinRNA-binding proteins (RBPs)extracellular vesicles (EVs) membrane vesicles (MVs)
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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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A PDCD1 Role in the Genetic Predisposition to NAFLD-HCC?

2021

Obesity and non-alcoholic fatty liver disease (NAFLD) are contributing to the global rise in deaths from hepatocellular carcinoma (HCC). The pathogenesis of NAFLD-HCC is not well understood. The severity of hepatic steatosis, steatohepatitis and fibrosis are key pathogenic mechanisms, but animal studies suggest altered immune responses are also involved. Genetic studies have so far highlighted a major role of gene variants promoting fat deposition in the liver (PNPLA3 rs738409

0301 basic medicineCancer ResearchCirrhosisprimary liver cancer<i>PDCD1</i>610 Medicine & healthDiseaseBioinformaticslcsh:RC254-282digestive systemArticleTM6SF2metabolic syndrome03 medical and health sciences0302 clinical medicinePD-1medicineGenetic predispositionPNPLA3business.industry<i>TM6SF2</i>PDCD1Fatty livernutritional and metabolic diseaseshepatocellular carcinomasingle-nucleotide polymorphismlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseasedigestive system diseases3. Good health<i>PNPLA3</i>030104 developmental biologyOncology030211 gastroenterology & hepatologyMetabolic syndromeSteatohepatitisSteatosisbusinessgenetic predispositionTM6SF2Cancers
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