Search results for "Melanoma"

showing 10 items of 650 documents

Indicaxanthin from Opuntia Ficus Indica (L. Mill) impairs melanoma cell proliferation, invasiveness, and tumor progression.

2018

Abstract Background: A strong, reciprocal crosstalk between inflammation and melanoma has rigorously been demonstrated in recent years, showing how crucial is a pro-inflammatory microenvironment to drive therapy resistance and metastasis. Purpose: We investigated on the effects of Indicaxanthin, a novel, anti-inflammatory and bioavailable phytochemical from Opuntia Ficus Indica fruits, against human melanoma both in vitro and in vivo. Study Design and Methods: The effects of indicaxanthin were evaluated against the proliferation of A375 human melanoma cell line and in a mice model of cutaneous melanoma. Cell proliferation was assessed by MTT assay, apoptosis by Annexin V-Fluorescein Isothio…

0301 basic medicine3003MaleSkin NeoplasmsPyridinesPyridinePhytochemicalsMelanoma ExperimentalPharmaceutical ScienceIndicaxanthinApoptosisBcl-2 B cell lymphoma gene-2 (Bcl-2)chemistry.chemical_compoundMice0302 clinical medicineOpuntia Ficus Indica (L.Mill)Settore BIO/10 - BiochimicaDrug DiscoveryCXCL1 chemokine (C-X-C motif) ligand 1MelanomaNF-κB nuclear factor kappa BMTT 3-[45-dimethyltiazol-2-yl]-25-diphenyl tetrazolium bromideMelanomaNF-kappa BOpuntiaComplementary and Alternative Medicine2708 DermatologyBetaxanthinsCXCL1030220 oncology & carcinogenesisMolecular MedicinePhC phytochemicalGrowth inhibitionIndicaxanthinHumanBiologyPhytochemicalNHEM normal human epidermal melanocyte03 medical and health sciencesc-FLIP FLICE-inhibitory proteinIn vivoCell Line TumormedicineAnimalsHumansNeoplasm InvasivenessSkin NeoplasmCell ProliferationNeoplasm InvasiveneInflammationPharmacologyCell growthAnimalDrug Discovery3003 Pharmaceutical ScienceApoptosimedicine.diseaseMice Inbred C57BL030104 developmental biologyComplementary and alternative medicinechemistryTumor progressionList of Abbrevations: AxV-FITC annexin V-fluorescein isothiocyanateBetaxanthinFruitCutaneous melanomaCancer researchPI propidium iodide PIPhytomedicine : international journal of phytotherapy and phytopharmacology
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Phase I Study of the Indoleamine 2,3-Dioxygenase 1 (IDO1) Inhibitor Navoximod (GDC-0919) Administered with PD-L1 Inhibitor (Atezolizumab) in Advanced…

2019

Abstract Purpose: IDO1 induces immune suppression in T cells through l-tryptophan (Trp) depletion and kynurenine (Kyn) accumulation in the local tumor microenvironment, suppressing effector T cells and hyperactivating regulatory T cells (Treg). Navoximod is an investigational small-molecule inhibitor of IDO1. This phase I study evaluated safety, tolerability, pharmacokinetics, and pharmacodynamics of navoximod in combination with atezolizumab, a PD-L1 inhibitor, in patients with advanced cancer. Patients and Methods: The study consisted of a 3+3 dose-escalation stage (n = 66) and a tumor-specific expansion stage (n = 92). Navoximod was given orally every 12 hours continuously for 21 consecu…

0301 basic medicineAdultCancer ResearchIndoles[SDV]Life Sciences [q-bio][SDV.BC]Life Sciences [q-bio]/Cellular BiologyPharmacologyAntibodies Monoclonal HumanizedArticleB7-H1 Antigen03 medical and health sciences0302 clinical medicinePharmacokineticsAtezolizumabRenal cell carcinomaNeoplasmsAntineoplastic Combined Chemotherapy ProtocolsmedicineBiomarkers TumorHumansIndoleamine-Pyrrole 23-DioxygenaseNeoplasm MetastasisAgedNeoplasm StagingAged 80 and overBladder cancerbusiness.industryMelanomaImidazolesMiddle Agedmedicine.diseaseMagnetic Resonance Imaging3. Good health030104 developmental biologyTreatment OutcomeOncologyTolerability030220 oncology & carcinogenesisPharmacodynamicsPD-L1 inhibitorbusinessTomography X-Ray Computed
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The Amount of Melanin Influences p16 Loss in Spitzoid Melanocytic Lesions: Correlation With CDKN2A Status by FISH and MLPA.

2019

AIMS The risk assessment of spitzoid lesions is one of the most difficult challenges in dermatopathology practice. In this regard, the loss of p16 expression and the homozygous deletion of CDKN2A, have been pointed in the literature as reliable indicators of high risk. However, these findings are poorly reproducible, and the molecular bases underlying the loss of p16 expression remain unclear. We aimed to identify the underlying events causing loss of CDKN2A/p16 in spitzoid tumors. MATERIALS AND METHODS We evaluated the immunohistochemical expression of p16, and the presence of CDKN2A genetic alterations detected through fluorescence in situ hybridization (FISH) and multiplex ligation-depen…

0301 basic medicineAdultMalePathologymedicine.medical_specialtyHistologySkin NeoplasmsPathology and Forensic MedicineMelanin03 medical and health sciencesYoung Adult0302 clinical medicineCDKN2ANevus Epithelioid and Spindle CellmedicineBiomarkers TumorNevusHumansMultiplex ligation-dependent probe amplificationneoplasmsMelanomaCyclin-Dependent Kinase Inhibitor p16In Situ Hybridization FluorescenceMelaninsmedicine.diagnostic_testbusiness.industryMelanomamedicine.diseaseImmunohistochemistryGene Expression Regulation NeoplasticMedical Laboratory Technology030104 developmental biology030220 oncology & carcinogenesisMutationImmunohistochemistryMelanocytesFemaleDermatopathologybusinessMultiplex Polymerase Chain ReactionFluorescence in situ hybridizationApplied immunohistochemistrymolecular morphology : AIMM
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Oxidative stress and antioxidants in the pathophysiology of malignant melanoma.

2018

Abstract The high number of somatic mutations in the melanoma genome associated with cumulative ultra violet (UV) exposure has rendered it one of the most difficult of cancers to treat. With new treatment approaches based on targeted and immune therapies, drug resistance has appeared as a consistent problem. Redox biology, including reactive oxygen and nitrogen species (ROS and RNS), plays a central role in all aspects of melanoma pathophysiology, from initiation to progression and to metastatic cells. The involvement of melanin production and UV radiation in ROS/RNS generation has rendered the melanocytic lineage a unique system for studying redox biology. Overall, an elevated oxidative st…

0301 basic medicineBiochemistry & Molecular BiologyClinical Biochemistrymedicine.disease_causeBiochemistryAntioxidantsMelanin03 medical and health scienceschemistry.chemical_compound0302 clinical medicineMedicineAnimalsHumanstumor microenvironmentEpigeneticsmetastasesMolecular BiologyMelanomaReactive nitrogen specieschemistry.chemical_classificationreactive oxygen speciesReactive oxygen speciesTumor microenvironmentskin cancerbusiness.industryMelanomaintracellular redox statemedicine.diseaseOxidative Stress030104 developmental biologyreactive nitrogen specieschemistry030220 oncology & carcinogenesisCancer researchBiochemistry and Cell BiologySkin cancerbusinessOxidation-ReductionOxidative stressSignal Transduction
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Molecular analysis of differential antiproliferative activity of resveratrol, epsilon viniferin and labruscol on melanoma cells and normal dermal cel…

2018

IF 3.778 (2016); International audience; Very recently, we have produced new resveratrol derived compounds, especially labruscol by culture of elicited grapevine cell suspensions (Vitis labrusca L.). This new polyphenolic oligomer could function as cancer chemopreventive agent in similar manner of resveratrol. In this study, we have determined the efficiency of resveratrol, ε-viniferin and the labruscol on human melanoma cell with or without metastatic phenotype. Our results show a differential activity of the three compounds where the resveratrol remains the polyphenolic compound with the most effective action compared to other oligomers. These three compounds block cell cycle of melanoma …

0301 basic medicineBioproductsProgrammed cell deathCellCyclin AResveratrolepsilon-ViniferinCell cycleToxicologyS Phase03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCell Line Tumor[SDV.IDA]Life Sciences [q-bio]/Food engineeringCDC2 Protein KinaseCyclin EStilbenesmedicineCytotoxic T cellAnticarcinogenic AgentsHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyCyclin D1VitisMelanoma cellsMelanomaCyclinBenzofuransCell ProliferationSkinKinaseCyclin-Dependent Kinase 2food and beveragesPolyphenolsGeneral MedicineCell cycleFibroblasts3. Good health030104 developmental biologymedicine.anatomical_structurechemistryResveratrol030220 oncology & carcinogenesis[SDV.TOX]Life Sciences [q-bio]/ToxicologyCancer researchFood ScienceFood and chemical toxicology : an international journal published for the British Industrial Biological Research Association
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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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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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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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Melanoma in the liver: Oxidative stress and the mechanisms of metastatic cell survival.

2020

Abstract Metastatic melanoma is a fatal disease with a rapid systemic dissemination. The most frequent target sites are the liver, bone, and brain. Melanoma metastases represent a heterogeneous cell population, which associates with genomic instability and resistance to therapy. Interaction of melanoma cells with the hepatic sinusoidal endothelium initiates a signaling cascade involving cytokines, growth factors, bioactive lipids, and reactive oxygen and nitrogen species produced by the cancer cell, the endothelium, and also by different immune cells. Endothelial cell-derived NO and H2O2 and the action of immune cells cause the death of most melanoma cells that reach the hepatic microvascul…

0301 basic medicineCancer ResearchEndotheliumCell SurvivalPopulationCellmedicine.disease_cause03 medical and health sciences0302 clinical medicineImmune systemDownregulation and upregulationTumor MicroenvironmentMedicineAnimalsHumansEndotheliumeducationMelanomaeducation.field_of_studybusiness.industryMelanomaLiver Neoplasmsmedicine.diseaseCarcinoma NeuroendocrineOxidative Stress030104 developmental biologymedicine.anatomical_structure030220 oncology & carcinogenesisCancer cellCancer researchbusinessOxidation-ReductionOxidative stressSeminars in cancer biology
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