Search results for "NOMA"

showing 10 items of 6328 documents

Rational Combination of Parvovirus H1 With CTLA-4 and PD-1 Checkpoint Inhibitors Dampens the Tumor Induced Immune Silencing

2019

The recent therapeutic success of immune checkpoint inhibitors in the treatment of advanced melanoma highlights the potential of cancer immunotherapy. Oncolytic virus-based therapies may further improve the outcome of these cancer patients. A human ex vivo melanoma model was used to investigate the oncolytic parvovirus H-1 (H-1PV) in combination with ipilimumab and/or nivolumab. The effect of this combination on activation of human T lymphocytes was demonstrated. Expression of CTLA-4, PD-1, and PD-L1 immune checkpoint proteins was upregulated in H-1PV-infected melanoma cells. Nevertheless, maturation of antigen presenting cells such as dendritic cells was triggered by H-1PV infected melanom…

0301 basic medicineCancer ResearchRegulatory T cellmedicine.medical_treatmentIpilimumablcsh:RC254-28203 medical and health sciences0302 clinical medicineimmune cellsCancer immunotherapymedicinemelanomaCytotoxic T cellipilimumabAntigen-presenting cellOriginal Researchnivolumabbusiness.industrylcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensImmune checkpointH-1PV030104 developmental biologymedicine.anatomical_structureOncologyCTLA-4030220 oncology & carcinogenesisCancer researchimmunotherapyNivolumabbusinessmedicine.drugFrontiers in Oncology
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HGF/MET Axis Induces Tumor Secretion of Tenascin-C and Promotes Stromal Rewiring in Pancreatic Cancer

2021

Simple Summary It has been previously shown that activation of the MET receptor by its ligand, the hepatocyte growth factor (HGF), modulates the tumor-stroma cross-talk in models of pancreatic cancer. We now wish to cast light on the molecular mechanisms by which this ligand/receptor pair sustains the interaction between cancer cells and the tumor microenviroment. To this end, we compared data obtained by large-scale analysis of gene expression in pancreatic cancer cells grown in the presence of HGF versus cells grown in the presence of HGF and treated with specific inhibitors of HGF/MET signaling. By clustering differentially expressed genes according to functional groups, we identified ca…

0301 basic medicineCancer ResearchStromal cellpancreatic ductal adenocarcinomaArticle03 medical and health sciences0302 clinical medicinePancreatic tumorPancreatic cancerMET oncogenemedicinetumor microenvironmentmetastasisHepatocyte growth factor; MET oncogene; Metastasis; Pancreatic ductal adenocarcinoma; Tenascin C; Tumor microenvironmentRC254-282Tumor microenvironmentbiologyChemistryTenascin Ctenascin CNeoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.disease030104 developmental biologyhepatocyte growth factorOncology030220 oncology & carcinogenesisCancer cellHepatic stellate cellbiology.proteinCancer researchHepatocyte growth factormedicine.drugCancers
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Melanoma Lesions Independently Acquire T-cell Resistance during Metastatic Latency

2016

Abstract Melanoma often recurs after a latency period of several years, presenting a T cell–edited phenotype that reflects a role for CD8+ T cells in maintaining metastatic latency. Here, we report an investigation of a patient with multiple recurrent lesions, where poorly immunogenic melanoma phenotypes were found to evolve in the presence of autologous tumor antigen–specific CD8+ T cells. Melanoma cells from two of three late recurrent metastases, developing within a 6-year latency period, lacked HLA class I expression. CD8+ T cell–resistant, HLA class I–negative tumor cells became clinically apparent 1.5 and 6 years into stage IV disease. Genome profiling by SNP arrays revealed that HLA …

0301 basic medicineCancer ResearchT cellmedicine.medical_treatmentMedizinHuman leukocyte antigenCD8-Positive T-LymphocytesBiology03 medical and health sciencesAntigens NeoplasmmedicineHumansNeoplasm MetastasisMelanomaMelanomaCancerImmunosuppressionmedicine.diseasePhenotypeNeoplasm Proteins030104 developmental biologymedicine.anatomical_structureOncologyLatency stageImmunologyCD8Cancer Research
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Targeting COPZ1 non-oncogene addiction counteracts the viability of thyroid tumor cells

2017

Abstract Thyroid carcinoma is generally associated with good prognosis, but no effective treatments are currently available for aggressive forms not cured by standard therapy. To find novel therapeutic targets for this tumor type, we had previously performed a siRNA-based functional screening to identify genes essential for sustaining the oncogenic phenotype of thyroid tumor cells, but not required to the same extent for the viability of normal cells (non-oncogene addiction paradigm). Among those, we found the coatomer protein complex ζ1 (COPZ1) gene, which is involved in intracellular traffic, autophagy and lipid homeostasis. In this paper, we investigated the mechanisms through which COPZ…

0301 basic medicineCancer ResearchTime FactorsCOPZ1ApoptosisCOPZ1Thyroid cancerThyroid NeoplasmThyroidRNAi TherapeuticCell death; COPZ1; Non-oncogene addiction; Thyroid carcinoma; Animals; Apoptosis; Autophagy; Cell Line Tumor; Cell Survival; Coatomer Protein; Endoplasmic Reticulum Stress; Female; Gene Expression Regulation Neoplastic; Humans; Mice Nude; RNA Interference; Signal Transduction; Thyroid Neoplasms; Time Factors; Transfection; Tumor Burden; Unfolded Protein Response; Xenograft Model Antitumor Assays; RNAi Therapeutics; Oncology; Cancer ResearchEndoplasmic Reticulum StressOncogene AddictionTumor BurdenGene Expression Regulation Neoplasticmedicine.anatomical_structureOncologyFemaleRNA InterferenceNon-oncogene addictionHumanSignal TransductionCell deathProgrammed cell deathXenograft Model Antitumor AssayTime FactorCell SurvivalMice NudeBiologyTransfectionCoatomer ProteinThyroid carcinomaThyroid carcinoma03 medical and health sciencesCell Line TumorAutophagymedicineAnimalsHumansThyroid NeoplasmsEndoplasmic Reticulum StreAnimalAutophagyApoptosimedicine.diseaseXenograft Model Antitumor AssaysRNAi Therapeutics030104 developmental biologyImmunologyUnfolded Protein ResponseCancer researchUnfolded protein response
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Chronic Sulforaphane Application Does Not Induce Resistance in Renal Cell Carcinoma Cells.

2018

Background/aim Since the natural compound sulforaphane (SFN) has been shown to stop tumor growth, renal cell carcinoma (RCC) patients often use this drug in addition to their prescribed oncotherapy. The aim of this study was to examine whether resistance to SFN may develop after long-term application. Materials and methods Several RCC cell lines were incubated with SFN for short periods of time (24-72 h) or long periods of time (8 weeks) and cell growth, proliferation, and cell-cycle proteins were analyzed. Results Both short- and long-term application of SFN distinctly reduced RCC cell growth and proliferation. However, differences in the distribution of cells in each phase of the cell cyc…

0301 basic medicineCancer ResearchTime FactorsCell SurvivalCell Cycle Proteins03 medical and health scienceschemistry.chemical_compoundIsothiocyanatesCell Line TumorAnticarcinogenic AgentsHumansPhosphorylationProtein kinase BCarcinoma Renal CellCell ProliferationCyclin-dependent kinase 1biologyCell growthCyclin-dependent kinase 2General MedicineCell cycleKidney NeoplasmsGene Expression Regulation Neoplastic030104 developmental biologyOncologychemistryCell cultureA549 CellsDrug Resistance NeoplasmSulfoxidesCancer researchbiology.proteinSignal transductionDrug Screening Assays AntitumorSulforaphaneSignal TransductionAnticancer research
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Artesunate Inhibits Growth of Sunitinib-Resistant Renal Cell Carcinoma Cells through Cell Cycle Arrest and Induction of Ferroptosis

2020

Although innovative therapeutic concepts have led to better treatment of advanced renal cell carcinoma (RCC), efficacy is still limited due to the tumor developing resistance to applied drugs. Artesunate (ART) has demonstrated anti-tumor effects in different tumor entities. This study was designed to investigate the impact of ART (1&ndash

0301 basic medicineCancer ResearchTraditional Chinese Medicine (TCM) growth inhibition ferroptosis reactive oxygen species (ROS)Cell cycle checkpointBiologyurologic and male genital diseasesreactive oxygen species (ROS)lcsh:RC254-282Articlegrowth inhibition03 medical and health scienceschemistry.chemical_compound0302 clinical medicinerenal cell carcinoma (RCC)medicineClonogenic assayCytotoxicityartesunate (ART)SunitinibTraditional Chinese Medicine (TCM)Cell cyclelcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensferroptosissunitib resistance030104 developmental biologyOncologychemistryCell cultureApoptosis030220 oncology & carcinogenesisCancer researchGrowth inhibitionmedicine.drugCancers
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Abstract CT156: A first-in-human phase I/II clinical trial assessing novel mRNA-lipoplex nanoparticles encoding shared tumor antigens for immunothera…

2018

Abstract Therapeutic vaccination with tumor antigen-encoding RNAs is being investigated in various clinical trials. Typically, the RNA vaccine is administered intradermally, subcutaneously or intranodally with the intention to get expression of the encoded antigens in local antigen-presenting cells (APCs). We have developed a novel class of RNA-lipoplex (RNA(LIP)) immunotherapeutics for intravenous application, which allow systemic targeting of APCs. RNA(LIP) is a novel nanoparticulate formulation of lipid-complexed mRNA which selectively delivers the functional mRNA to APCs in lymphoid compartments body-wide for efficient mRNA uptake and expression of the encoded antigen by APCs. Moreover,…

0301 basic medicineCancer Researchbusiness.industrymedicine.medical_treatmentMelanomaImmunogenicityImmunotherapymedicine.diseaseVaccination03 medical and health sciences030104 developmental biology0302 clinical medicineImmune systemOncologyAntigen030220 oncology & carcinogenesisImmunologyMedicineCancer vaccinebusinessAdjuvantCancer Research
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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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Abilities of β-Estradiol to interact with chemotherapeutic drugs, signal transduction inhibitors and nutraceuticals and alter the proliferation of pa…

2019

Improving the effects of chemotherapy and reducing the side effects are important goals in cancer research. Various approaches have been examined to enhance the effectiveness of chemotherapy. For example, signal transduction inhibitors or hormonal based approaches have been included with chemo- or radio-therapy. MIA-PaCa-2 and BxPC-3 pancreatic ductal adenocarcinoma (PDAC) cells both express the estrogen receptor (ER). The effects of β-estradiol on the growth of PDAC cells has not been examined yet the ER is expressed in PDAC cells. We have examined the effects of combining β-estradiol with chemotherapeutic drugs, signal transcription inhibitors, natural products and nutraceuticals on PDAC.…

0301 basic medicineCancer Researchendocrine system diseasesβ estradiolmedicine.medical_treatmentβ-EstradiolEstrogen receptorAntineoplastic AgentsNatural product03 medical and health sciencesFood-Drug Interactions0302 clinical medicineNutraceuticalPancreatic cancerCell Line TumorGeneticsmedicineHumansMolecular BiologyChemotherapeutic drugCell ProliferationChemotherapyNatural products?-EstradiolEstradiolbusiness.industryQUIMIOTERÁPICOSChemotherapeutic drugs; Natural products; Nutraceuticals; Pancreatic cancer; β-EstradiolPancreatic cancerMiddle Agedmedicine.diseasedigestive system diseasesPancreatic Neoplasms030104 developmental biology030220 oncology & carcinogenesisDietary SupplementsCancer researchSettore BIO/14 - FarmacologiaMolecular MedicineChemotherapeutic drugsFemaleChemotherapeutic drugsNutraceuticalsNutraceuticalSignal transductionbusinessHormoneCarcinoma Pancreatic DuctalSignal TransductionAdvances in biological regulation
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