Search results for "Format"

showing 10 items of 24643 documents

Establishment and characterization of a highly immunogenic human renal carcinoma cell line.

2015

Renal cell carcinoma (RCC) is the most common kidney cancer, and accounts for ~3% of all adult malignancies. RCC has proven refractory to conventional treatment modalities but appears to be the only histological form that shows any consistent response to immunotherapeutic approaches. The development of a clinically effective vaccine remains a major strategic target for devising active specific immunotherapy in RCC. We aimed to identify a highly immunogenic antigenic format for immunotherapeutic approaches, so as to boost immune responses in RCC patients. We established and cloned an immunogenic cell line, RCC85#21 named Elthem, which was derived from a non-aggressive and non-metastatic clea…

0301 basic medicineCancer ResearchCellClone (cell biology)BiologyImmunophenotyping03 medical and health sciencesimmunogenic antigenic format0302 clinical medicineImmune systemAntigenAntigens NeoplasmCell Line TumormedicineCytotoxic T cellHumansElectrophoresis Gel Two-DimensionalCarcinoma Renal Cellrenal cancer cell lineSystems BiologyArticlesCell cycleMolecular biologyKidney Neoplasms030104 developmental biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesisSpectrometry Mass Matrix-Assisted Laser Desorption-Ionizationcell proteomeClear cell carcinomaK562 CellsCD8International journal of 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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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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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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Conceptual framework for precision cancer medicine in Germany: Consensus statement of the Deutsche Krebshilfe working group ‘Molecular Diagnostics an…

2020

Precision cancer medicine (PCM) holds great promises to offer more effective therapies to patients based on molecular profiling of their individual tumours. Although the PCM approach seems intuitive, multiple conceptional and structural challenges interfere with the broad implementation of PCM into clinical practice. Accordingly, concerted national and international efforts are needed to guide the further development and broad adoption of PCM in Germany. With support of the 'German Cancer Aid' (Deutsche Krebshilfe [DKH]) a task force 'Molecular Diagnostics and Therapy' was implemented. In two workshops supported by the DKH, delegates from the fourteen comprehensive cancer centresidentified …

0301 basic medicineCancer ResearchCollaborative strategyConsensusDelphi TechniqueComputer scienceMedizinAntineoplastic AgentsComputer-assisted web interviewing03 medical and health sciences0302 clinical medicineCancer MedicinePredictive Value of TestsGermanyNeoplasmsHumansProfiling (information science)Molecular Targeted TherapyPrecision MedicineTask forceMolecular diagnosticsPrecision medicineEngineering management030104 developmental biologyMolecular Diagnostic TechniquesOncologyConceptual frameworkResearch Design030220 oncology & carcinogenesisEuropean Journal of Cancer
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Long Pentraxin 3-Mediated Fibroblast Growth Factor Trapping Impairs Fibrosarcoma Growth

2018

Fibrosarcomas are soft tissue mesenchymal tumors originating from transformed fibroblasts. Fibroblast growth factor-2 (FGF2) and its tyrosine-kinase receptors (FGFRs) play pivotal roles in fibrosarcoma onset and progression, FGF2 being actively produced by fibroblasts in all stages along their malignant transformation to the fibrosarcoma stage. The soluble pattern recognition receptor long pentraxin-3 (PTX3) is an extrinsic oncosuppressor whose expression is reduced in different tumor types, including soft tissue sarcomas, via hypermethylation of its gene promoter. PTX3 interacts with FGF2 and other FGF family members, thus acting as a multi-FGF antagonist able to inhibit FGF-dependent neov…

0301 basic medicineCancer ResearchFGF; FGF-trap; FGFR; fibrosarcoma; long pentraxin-3Fibroblast growth factorlcsh:RC254-282Malignant transformation03 medical and health sciences0302 clinical medicinemedicineFGFFibrosarcomaFibroblastReceptorneoplasmsOriginal ResearchFGF-trapintegumentary systemChemistryFGFRMesenchymal stem cellPTX3medicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens030104 developmental biologymedicine.anatomical_structurelong pentraxin-3OncologyFibroblast growth factor receptor030220 oncology & carcinogenesisCancer researchfibrosarcomaFrontiers in Oncology
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Tumour mutational burden as a biomarker for immunotherapy: Current data and emerging concepts

2020

International audience; Treatment with immune checkpoint inhibitors targeting programmed cell death protein 1 (PD-1) or its ligand (PD-L1) can generate durable responses in various cancer types, but only in a subset of patients. The use of predictive biomarkers for response to PD-1/PD-L1 inhibitors is critical for patient selection. Expression of PD-L1 has demonstrated utility in patient selection. Tumour mutational burden (TMB) is an emerging biomarker for response to PD-1/PD-L1 inhibitors. The evaluation of this biomarker is based on the hypothesis that a high number of mutations in somatic exonic regions will lead to an increase in neoantigen production, which could then be recognised by…

0301 basic medicineCancer ResearchImmune checkpoint inhibitorsmedicine.medical_treatment[SDV]Life Sciences [q-bio]DNA Mutational AnalysisProgrammed Cell Death 1 ReceptorTumour mutational burdenBioinformaticsArticleB7-H1 Antigen03 medical and health sciencesAntineoplastic Agents Immunological0302 clinical medicineImmune systemNeoplasmsBiomarkers TumorHumansMedicineIn patientGenetic TestingPredictive biomarkerbusiness.industryPatient SelectionCancerBiomarkerImmunotherapymedicine.disease3. Good healthBiomarker (cell)[SDV] Life Sciences [q-bio]030104 developmental biologyOncologyDrug Resistance Neoplasm030220 oncology & carcinogenesisMutationImmunotherapybusinessCD8
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Immunotherapy in non-small-cell lung cancer: a bridge between research and clinical practice

2018

Lung cancer has been historically considered a poorly immunogenic disease because of the few evidence of immune responses in affected patients and the limited efficacy of immunomodulating strategies. Recent understanding of the molecular mechanisms leading to cancer immune evasion has allowed the development of a new class of drugs called immune checkpoint inhibitors, which reactivate host responses with outstanding clinical benefits in a portion of patients with non-small-cell lung cancer. In this review, we briefly summarize the basis of immunogenicity and immune escape of cancer, with specific focus on non-small-cell lung cancer, mechanisms underlying immune checkpoint inhibitors effica…

0301 basic medicineCancer ResearchLung NeoplasmsSettore MED/06 - Oncologia Medicamedicine.medical_treatmentProgrammed Cell Death 1 Receptorimmune checkpoint inhibitorDiseaseNSCLCBioinformaticsB7-H1 Antigenimmune checkpoint inhibitorsTranslational Research Biomedical0302 clinical medicineCarcinoma Non-Small-Cell LungPD-1clinical studiesNSCLC; PD-1; PD-L1; biomarkers; cancer immunogenicity; clinical studies; immune checkpoint inhibitors; translational researchMolecular Targeted TherapybiologyImmunogenicityGeneral Medicinecancer immunogenicityOncology030220 oncology & carcinogenesisbiomarkerCytokinesImmunotherapyPD-L1chemical and pharmacologic phenomena03 medical and health sciencesLymphocytes Tumor-InfiltratingImmune systemPD-L1Biomarkers TumormedicineHumansLung cancerbusiness.industryImmunitybiomarkersCancerImmunotherapymedicine.disease030104 developmental biologytranslational researchTumor EscapeMutationbiology.proteinTumor Escapebusinessclinical studieFuture Oncology
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Concepts to Target MYC in Pancreatic Cancer.

2016

Abstract Current data suggest that MYC is an important signaling hub and driver in pancreatic ductal adenocarcinoma (PDAC), a tumor entity with a strikingly poor prognosis. No targeted therapies with a meaningful clinical impact were successfully developed against PDAC so far. This points to the need to establish novel concepts targeting the relevant drivers of PDAC, like KRAS or MYC. Here, we discuss recent developments of direct or indirect MYC inhibitors and their potential mode of action in PDAC. Mol Cancer Ther; 15(8); 1792–8. ©2016 AACR.

0301 basic medicineCancer ResearchPoor prognosisPancreatic ductal adenocarcinomaendocrine system diseasesGene regulatory networkAntineoplastic AgentsBiologymedicine.disease_causeBioinformaticsProto-Oncogene Proteins c-myc03 medical and health sciencesPancreatic cancerCarcinomamedicineAnimalsHumansGene Regulatory NetworksMolecular Targeted TherapyProtein Kinase InhibitorsCancerGenetic Variationmedicine.diseasedigestive system diseasesGene Expression Regulation NeoplasticPancreatic Neoplasms030104 developmental biologyOncologyCarrier proteinCancer researchKRASCarrier ProteinsCarcinoma Pancreatic DuctalProtein BindingSignal TransductionMolecular cancer therapeutics
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Preclinical models for precision oncology

2018

Precision medicine approaches have revolutionized oncology. Personalized treatments require not only identification of the driving molecular alterations, but also development of targeted therapies and diagnostic tests to identify the appropriate patient populations for clinical trials and subsequent therapeutic implementation. Preclinical in vitro and in vivo models are widely used to predict efficacy of newly developed treatments. Here we discuss whether, and to what extent, preclinical models including cell lines, organoids and tumorgrafts recapitulate key features of human tumors. The potential of preclinical models to anticipate treatment efficacy and clinical benefit is also presented,…

0301 basic medicineCancer ResearchPreclinical modelsMedical OncologyBioinformaticsModels Biological03 medical and health sciences0302 clinical medicineCell Line TumorNeoplasmsGeneticsAnimalsHumansMedicinePrecision Medicinebusiness.industryOrganoids; Patient-derived xenografts (PDX); Preclinical models; Oncology; Genetics; Cancer ResearchDiagnostic testPrecision medicineKey featuresTreatment efficacy3. Good healthClinical trialOrganoids030104 developmental biologyOncologyPrecision oncologyPatient-derived xenografts (PDX)030220 oncology & carcinogenesisHeterograftsbusinessBiochimica et Biophysica Acta (BBA) - Reviews on Cancer
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