Search results for "NOMA"

showing 10 items of 6328 documents

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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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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Knockdown of hnRNPK leads to increased DNA damage after irradiation and reduces survival of tumor cells.

2017

Radiotherapy is an important treatment option in the therapy of multiple tumor entities among them head and neck squamous cell carcinoma (HNSCC). However, the success of radiotherapy is limited by the development of radiation resistances. Heterogeneous nuclear ribonucleoprotein K (hnRNPK) is a cofactor of p53 and represents a potential target for radio sensitization of tumor cells. In this study, we analyzed the impact of hnRNPK on the DNA damage response after gamma irradiation. By yH2AX foci analysis, we found that hnRNPK knockdown increases DNA damage levels in irradiated cells. Tumor cells bearing a p53 mutation showed increased damage levels and delayed repair. Knockdown of hnRNPK appl…

0301 basic medicineCancer ResearchDNA damageCell Survivalmedicine.medical_treatmentmedicine.disease_causeRadiation ToleranceHeterogeneous-Nuclear Ribonucleoprotein KHistones03 medical and health sciences0302 clinical medicineCell Line TumormedicineCarcinomaGene Knockdown TechniquesHumansMutationGene knockdownChemistrySquamous Cell Carcinoma of Head and NeckStem CellsGeneral Medicinemedicine.diseaseHead and neck squamous-cell carcinomaRadiation therapy030104 developmental biologyCell cultureHead and Neck Neoplasms030220 oncology & carcinogenesisGene Knockdown TechniquesCancer researchCarcinoma Squamous CellTumor Suppressor Protein p53DNA DamageCarcinogenesis
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Targeting prohibitins with chemical ligands inhibits KRAS-mediated lung tumours.

2017

KRAS is one of the most frequently mutated oncogenes in human non-small cell lung cancers (NSCLCs). RAS proteins trigger multiple effector signalling pathways including the highly conserved RAF-MAPK pathway. CRAF, a direct RAS effector protein, is required for KRAS-mediated tumourigenesis. Thus, the molecular mechanisms driving the activation of CRAF are intensively studied. Prohibitin 1 (PHB1) is an evolutionarily conserved adaptor protein and interaction of CRAF with PHB1 at the plasma membrane is essential for CRAF activation. Here, we demonstrate that PHB1 is highly expressed in NSCLC patients and correlates with poor survival. Targeting of PHB1 with two chemical ligands (rocaglamide an…

0301 basic medicineCancer ResearchEGF Family of ProteinsLung NeoplasmsBiologyLigandsProto-Oncogene Proteins p21(ras)03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineGrowth factor receptorRocaglamideEpidermal growth factorCarcinoma Non-Small-Cell LungCell Line TumorProhibitinsGeneticsAnimalsHumansMolecular Targeted TherapyProhibitinMolecular BiologyBenzofuransCell ProliferationRas InhibitorMice KnockoutTNF Receptor-Associated Factor 3EffectorXenograft Model Antitumor Assaysrespiratory tract diseasesCell biologyProto-Oncogene Proteins p21(ras)Gene Expression Regulation NeoplasticRepressor Proteins030104 developmental biologychemistry030220 oncology & carcinogenesisras Proteinsraf KinasesSignal transductionSignal TransductionOncogene
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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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Growth differentiation factor 15 as a radiation-induced marker in oral carcinoma increasing radiation resistance.

2015

Background Growth differentiation factor 15 (GDF15) is involved in tumor pathogenesis of oral squamous cell carcinoma (OSCC). The aim of this study was an investigation of the potential influence of GDF15 on radioresistance of OSCC cells in vitro. Methods Oral squamous cell carcinoma cell lines were irradiated with 0, 2, or 6 Gy, and GDF15 expression in the supernatant per survived cell colony was examined with ELISA. Non-irradiated and OSCC cell lines irradiated with 6 Gy were evaluated for GDF15 expression using immunofluorescent staining. For further investigation of GDF15 effects on radioresistance, a GDF15 knockdown model in a human OSCC cell line was established, and apoptotic activit…

0301 basic medicineCancer ResearchGrowth Differentiation Factor 15CellApoptosisEnzyme-Linked Immunosorbent AssayBiologymedicine.disease_causeReal-Time Polymerase Chain ReactionTransfectionPathology and Forensic Medicine03 medical and health sciences0302 clinical medicineRadioresistanceCell Line TumormedicineCarcinomaBiomarkers TumorHumansRNA Small InterferingMouth neoplasmSquamous Cell Carcinoma of Head and Neckmedicine.diseaseMolecular biologyNeoplasm Proteinsstomatognathic diseases030104 developmental biologymedicine.anatomical_structureOtorhinolaryngologyApoptosisCell cultureTumor progressionHead and Neck Neoplasms030220 oncology & carcinogenesisCaspasesGene Knockdown TechniquesCarcinoma Squamous CellPeriodonticsMouth NeoplasmsOral SurgeryCarcinogenesisJournal of oral pathologymedicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology
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Prospective Image Quality and Lesion Assessment in the Setting of MR-Guided Radiation Therapy of Prostate Cancer on an MR-Linac at 1.5 T: A Compariso…

2021

The objective of this study is to conduct a qualitative and a quantitative image quality and lesion evaluation in patients undergoing MR-guided radiation therapy (MRgRT) for prostate cancer on a hybrid magnetic resonance imaging and linear accelerator system (MR-Linac or MRL) at 1.5 Tesla. This prospective study was approved by the institutional review board. A total of 13 consecutive patients with biopsy-confirmed prostate cancer and an indication for MRgRT were included. Prior to radiation therapy, each patient underwent an MR-examination on an MRL and on a standard MRI scanner at 3 Tesla (MRI3T). Three readers (two radiologists and a radiation oncologist) conducted an independent qualita…

0301 basic medicineCancer ResearchIntraclass correlationImage qualityPIRADSFleiss' kappalcsh:RC254-282ArticleLesion03 medical and health sciences0302 clinical medicineimage qualityMedicineEffective diffusion coefficientimage guidanceRadiation oncologistMR-Linacmedicine.diagnostic_testbusiness.industryMagnetic resonance imaginglcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogenslesion detection030104 developmental biologyadaptive radiotherapyOncologyprostate carcinoma030220 oncology & carcinogenesismpMRImedicine.symptombusinessNuclear medicineKappaCancers
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Doxorubicin anti-tumor mechanisms include Hsp60 post-translational modifications leading to the Hsp60/p53 complex dissociation and instauration of re…

2017

Hsp60 is a pro-carcinogenic chaperonin in certain tumor types by interfering with apoptosis and with tumor cell death. In these tumors, it is not known whether or not doxorubicin anti-tumor effects include a blockage of the pro-carcinogenic action of this protein. We used the human lung mucoepidermoid cell line NCI-H292 and different doses of doxorubicin to measure cell viability, cell cycle progression, cell senescence indicators, Hsp60 levels and its post-translational modifications as well as the release of the chaperonin into the extracellular environment. Cell viability was reduced in relation to doxorubicin dose and this was paralleled by the appearance of cell senescence markers. Con…

0301 basic medicineCancer ResearchLung NeoplasmsChaperoninsCellApoptosismedicine.disease_causeHistones0302 clinical medicineCellular SenescenceAntibiotics AntineoplasticAcetylationG2 Phase Cell Cycle Checkpointsmedicine.anatomical_structureOncology030220 oncology & carcinogenesisCell agingIntracellularProtein BindingSignal TransductionSenescenceCyclin-Dependent Kinase Inhibitor p21animal structuresCell Survivalchemical and pharmacologic phenomenaBiologycomplex mixturesMitochondrial ProteinsDoxorubicin Hsp60 Acetylation Ubiquitination p53 Replicative senescence03 medical and health sciencesDoxorubicin; Hsp60; p53; replicative senescence; post-translational modificationsCell Line TumormedicineHumansCell Proliferationdoxorubicin p53 Hsp60Dose-Response Relationship DrugCell growthfungiUbiquitinationChaperonin 60Molecular biology030104 developmental biologyAcetylationApoptosisDoxorubicinProteolysisCancer researchCarcinoma MucoepidermoidTumor Suppressor Protein p53CarcinogenesisProtein Processing Post-Translational
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NGS‐based liquid biopsy profiling identifies mechanisms of resistance to ALK inhibitors: a step toward personalized NSCLC treatment

2021

Despite impressive and durable responses, nonsmall cell lung cancer (NSCLC) patients treated with anaplastic lymphoma kinase (ALK) inhibitors (ALK‐Is) ultimately progress due to development of resistance. Here, we have evaluated the clinical utility of circulating tumor DNA (ctDNA) profiling by next‐generation sequencing (NGS) upon disease progression. We collected 26 plasma and two cerebrospinal fluid samples from 24 advanced ALK‐positive NSCLC patients at disease progression to an ALK‐I. These samples were analyzed by NGS and digital PCR. A tool to retrieve variants at the ALK locus was developed (VALK tool). We identified at least one resistance mutation in the ALK locus in ten (38.5%) p…

0301 basic medicineCancer ResearchLung NeoplasmsEML4-ALKAntineoplastic AgentsEML4‐ALKmedicine.disease_causeNSCLCIDH2Circulating Tumor DNA03 medical and health sciencesALK-TKI0302 clinical medicineCarcinoma Non-Small-Cell LungMAP2K1hemic and lymphatic diseasesALK‐TKIGeneticsmedicineHumansAnaplastic lymphoma kinaseAnaplastic Lymphoma KinaseDigital polymerase chain reactionPrecision MedicineLiquid biopsyProtein Kinase InhibitorsneoplasmsResearch ArticlesRC254-282MutationCrizotinibliquid biopsybusiness.industryHigh-Throughput Nucleotide SequencingNeoplasms. Tumors. Oncology. Including cancer and carcinogensGeneral MedicineResistance mutation3. Good health030104 developmental biologyOncologyDrug Resistance Neoplasm030220 oncology & carcinogenesisNGSMutationCancer researchMolecular MedicinebusinessResearch Articlemedicine.drugMolecular Oncology
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