Search results for "model."

showing 10 items of 23664 documents

Inhibition of colon cancer growth by docosahexaenoic acid involves autocrine production of TNFα

2016

IF 7.932; International audience; The omega-3 polyunsaturated fatty acid docosahexaenoic acid (DHA) has anti-inflammatory and anti-cancer properties. Among pro-inflammatory mediators, tumor necrosis factor a (TNF alpha) plays a paradoxical role in cancer biology with induction of cancer cell death or survival depending on the cellular context. The objective of the study was to evaluate the role of TNFa in DHA-mediated tumor growth inhibition and colon cancer cell death. The treatment of human colorectal cancer cells, HCT-116 and HCT-8 cells, with DHA triggered apoptosis in autocrine TNF alpha-dependent manner. We demonstrated that DHA-induced increased content of TNF alpha mRNA occurred thr…

0301 basic medicineCancer ResearchTumoricidal ActionApoptosis[ SDV.CAN ] Life Sciences [q-bio]/CancerMice[ SDV.GEN.GH ] Life Sciences [q-bio]/Genetics/Human geneticsForkhead Box Protein O3Cell cycle3. Good healthCell biologyGene Expression Regulation NeoplasticAutocrine CommunicationColonic NeoplasmsTumor-Necrosis-FactorTumor necrosis factor alphaProgrammed cell deathDocosahexaenoic AcidsHuman Colorectal-CancerGene-Expression[SDV.CAN]Life Sciences [q-bio]/Cancer[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiology03 medical and health sciencesGrowth factor receptorLipid-MetabolismGeneticsmedicineAnimalsHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyCell-DeathPolyunsaturated Fatty-AcidsAutocrine signallingMolecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyActivated Protein-KinaseTumor Necrosis Factor-alpha[ SDV.BC ] Life Sciences [q-bio]/Cellular BiologyInduced ApoptosisCancerHCT116 Cellsmedicine.diseaseXenograft Model Antitumor AssaysMicroRNAs030104 developmental biology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsApoptosisCancer cellCancer researchPrevents Breast-Cancer
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Cadmium-Associated Molecular Signatures in Cancer Cell Models

2021

Simple Summary The exposure of cancer cells to cadmium compounds may be associated with the acceleration of tumor progression. It is known that cadmium is a transcriptional regulator, and the study of differentially expressed genes has enabled the identification and classification of cadmium-associated molecular signatures as useful biomarkers that are potentially transferable to clinical research. This review recapitulates the studies that report the detection of such signatures in breast, gastric, colon, liver, lung, and nasopharyngeal tumor cell models, as specifically demonstrated by individual gene or whole genome expression profiling. Abstract The exposure of cancer cells to cadmium a…

0301 basic medicineCancer Researchcadmiumnasopharyngeal cancerReviewBiologygene signaturedifferential expressionliver cancer03 medical and health sciences0302 clinical medicinebreast cancerGene silencingSettore BIO/06 - Anatomia Comparata E CitologiaRC254-282Regulation of gene expressiongastric cancerNeoplasms. Tumors. Oncology. Including cancer and carcinogensGene signaturein vitro cell modelsPhenotypein vitro cell modelGene expression profilinglung cancer030104 developmental biologyOncologycolon cancerTumor progression030220 oncology & carcinogenesisCancer cellCancer researchReprogrammingCancers
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The hallmarks of ovarian cancer: proliferation and cell growth

2020

Epithelial ovarian cancer (EOC) is a heterogeneous group of diseases with distinct biological and clinical behaviour. Despite the differences between them, the capability of tumour cells to continuously proliferate and avoid death is maintained among histotypes. This ability is the result of alterations at different levels, causing the deregulation of cell cycle and proliferative-related pathways. Even if the leading role is played by RB and TP53, changes in other molecular pathways are involved in the development of EOC. This ability can be exploited to generate in vitro and in vivo models resembling the conditions of tumour development in a patient. In vivo models, such as patient-derived…

0301 basic medicineCancer Researchendocrine system diseaseslcsh:MedicineBiologylcsh:RC254-282Article03 medical and health sciencesCell growth0302 clinical medicinemedicineEpithelial ovarian cancerCell proliferationHeterogeneous groupCell growthlcsh:RCell cycleEpithelial ovarian cancerlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseAnimal models030104 developmental biologyOncologyTumour development030220 oncology & carcinogenesisGenetically Engineered MouseCancer researchOvarian cancerEJC Supplements
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Identification of clinical phenotypes and related survival in patients with large hccs

2021

Background. Hepatocellular carcinoma (HCC) factors, especially maximum tumor diameter (MTD), tumor multifocality, portal vein thrombosis (PVT), and serum alpha-fetoprotein (AFP), influence survival. Aim. To examine patterns of tumor factors in large HCC patients. Methods. A database of large HCC patients was examined. Results. A multiple Cox proportional hazard model on death identified low serum albumin levels and the presence of PVT and multifocality, with each having a hazard ratio ≥2.0. All combinations of these three parameters were examined in relation to survival. Using univariate Cox analysis, the combination of albumin &gt

0301 basic medicineCancer Researchmedicine.medical_specialtyPVTSettore MED/12 - GASTROENTEROLOGIASerum albuminlcsh:RC254-282GastroenterologyArticle03 medical and health sciences0302 clinical medicineInternal medicineMedicinePlateletHCCneoplasmsSurvival ratePVT.biologybusiness.industryProportional hazards modelAlbuminHazard ratioSettore MED/09 - MEDICINA INTERNAAlbuminMultifocalityHCC; large; phenotypes; PVT; multifocality; albuminlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseasedigestive system diseasesPortal vein thrombosisAlbumin; HCC; Large; Multifocality; Phenotypes; PVTPhenotypesPhenotype030104 developmental biologyOncology030220 oncology & carcinogenesisHepatocellular carcinomabiology.proteinLargebusiness
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Tumor Microenvironment And Epithelial Mesenchymal Transition As Targets To Overcome Tumor Multidrug Resistance

2020

It is well established that multifactorial drug resistance hinders successful cancer treatment. Tumor cell interactions with the tumor microenvironment (TME) are crucial in epithelial-mesenchymal transition (EMT) and multidrug resistance (MDR). TME-induced factors secreted by cancer cells and cancer-associated fibroblasts (CAFs) create an inflammatory microenvironment by recruiting immune cells. CD11b+/Gr-1+ myeloid-derived suppressor cells (MDSCs) and inflammatory tumor associated macrophages (TAMs) are main immune cell types which further enhance chronic inflammation. Chronic inflammation nurtures tumor-initiating/cancer stem-like cells (CSCs), induces both EMT and MDR leading to tumor re…

0301 basic medicineCancer Researchmedicine.medical_treatmentMultidrug resistanceTargeted therapyTargeted therapy0302 clinical medicineCancer-Associated FibroblastsNeoplasmsAntineoplastic Combined Chemotherapy ProtocolsTumor-Associated MacrophagesTumor MicroenvironmentPharmacology (medical)HypoxiaTOR Serine-Threonine KinasesSmall moleculesChemotherapy ; Hypoxia ; Inflammation ; Microenvironment ; Multidrug resistance ; Small molecules ; Targeted therapy.Drug Resistance Multiple3. Good healthDNA DemethylationGene Expression Regulation NeoplasticInfectious DiseasesOncology030220 oncology & carcinogenesisInflammation MediatorsEpithelial-Mesenchymal TransitionStromal cellMicroenvironmentBiologyProinflammatory cytokine03 medical and health sciencesCell Line TumormedicineAnimalsHumansChemotherapyEpithelial–mesenchymal transitionPharmacologyInflammationTumor microenvironmentCancerHypoxia-Inducible Factor 1 alpha Subunitmedicine.diseaseHistone Deacetylase InhibitorsMultiple drug resistanceDisease Models Animal030104 developmental biologyDrug Resistance NeoplasmCancer cellCancer research
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A Set of Cell Lines Derived from a Genetic Murine Glioblastoma Model Recapitulates Molecular and Morphological Characteristics of Human Tumors

2021

Simple Summary Glioblastoma (GBM) is a highly aggressive and almost inevitably lethal brain tumor. Animal models for GBM are crucial to study how the tumor evolves in vivo and to test novel treatment options. Most currently available models are based on the transplantation of human GBM cells into mice with a defective immune system. However, this approach does not allow to study the contribution of immune cells to GBM growth and to test immunotherapies. Transplantation of murine GBM cells overcomes this limitation, however, up to now, only a limited number, which mostly do not mimic important characteristics of human GBM, have been available. Via in vivo passaging, we established a set of m…

0301 basic medicineCancer Researchmouse modelCentral nervous systemBrain tumorBiologylcsh:RC254-282GenomeArticleTranscriptome03 medical and health sciences0302 clinical medicineIn vivoGliomamedicinePTENsyngeneic cell lineglioblastomalcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseasenervous system diseases030104 developmental biologymedicine.anatomical_structureOncologyCell culture030220 oncology & carcinogenesisCancer researchbiology.proteinCancers
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Ligand-dependent Hedgehog pathway activation in Rhabdomyosarcoma : the oncogenic role of the ligands

2017

Altres ajuts: This work was supported by grants from Institut Català d'Oncologia (ICO), Instituto de Salud Carlos III (RTICC-RD12/0036/0016, /0020, /0035, /0057; and PI14/00647), Fundació A BOSCH, Fundació Amics Joan Petit, ajuts predoctorals del VHIR and RIS3CAT grants COMRDI15-1-0014 (ACCIÓ and FEDER). Altres ajuts: FEDER/COMRDI15-1-0014 Rhabdomyosarcoma (RMS) is the most common type of soft tissue sarcoma in children. The Hedgehog (HH) pathway is known to develop an oncogenic role in RMS. However, the molecular mechanism that drives activation of the pathway in RMS is not well understood. The expression of HH ligands was studied by qPCR, western blot and immunohistochemistry. Functional …

0301 basic medicineCancer ResearchsarcomaCarcinogenesisVismodegibRhabdomyosarcoma; Hedgehog; vismodegib; UPR; TRIB3; sarcoma; cancerVismodegib610ApoptosisMice SCIDUPRLigandsMice03 medical and health sciences0302 clinical medicineCell MovementvismodegibRhabdomyosarcomaTumor Cells CulturedmedicinecancerAnimalsHumansHedgehog ProteinsAutocrine signallingRhabdomyosarcomaHedgehogCell ProliferationCancerChemistryTRIB3Sarcomamedicine.diseaseXenograft Model Antitumor AssaysHedgehog signaling pathway3. Good health030104 developmental biologyOncology030220 oncology & carcinogenesisUnfolded protein responseCancer researchFemaleSignal transductionTranslational TherapeuticsSmoothenedHedgehogSignal TransductionTranscription Factorsmedicine.drug
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Epigenetic Regulation of TRAIL Signaling: Implication for Cancer Therapy

2019

International audience; One of the main characteristics of carcinogenesis relies on genetic alterations in DNA and epigenetic changes in histone and non-histone proteins. At the chromatin level, gene expression is tightly controlled by DNA methyl transferases, histone acetyltransferases (HATs), histone deacetylases (HDACs), and acetyl-binding proteins. In particular, the expression level and function of several tumor suppressor genes, or oncogenes such as c-Myc, p53 or TRAIL, have been found to be regulated by acetylation. For example, HATs are a group of enzymes, which are responsible for the acetylation of histone proteins, resulting in chromatin relaxation and transcriptional activation,…

0301 basic medicineCancer Researchtumor necrosis factor (TNF)TRAILReviewmedicine.disease_causelcsh:RC254-282Chromatin remodelingchromatin remodeling03 medical and health sciences0302 clinical medicinemedicinetumor necrosis factor (TNF).[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular Biologycancer[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyEpigeneticsHistone Acetyltransferasesbiologyhistone deacetylase (HDAC)lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens3. Good healthChromatin030104 developmental biologyHistonehistone deacetylase inhibitors (HDACIs)OncologyAcetylation030220 oncology & carcinogenesissilencingCancer researchbiology.proteinHistone deacetylasemethylationCarcinogenesisCancers
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Red wine extract disrupts Th17 lymphocyte differentiation in a colorectal cancer context

2020

International audience; Scope: Scope: It is well established that immune response and inflammation promote tumoral progression. Immune cells communicate through direct contact or through cytokine secretion, and it is the pro-inflammatory status that will tip the balance toward tumor progression or anti-tumor immunity. It is demonstrated here that a red wine extract (RWE) can decrease inflammation through its action on the inflammasome complex. This study determines whether an RWE could impact other key actors of inflammation, including T helper 17 (Th17) immune cells in particular. Methods and results: Methods and results: Using an RWE containing 4.16 g of polyphenols/liter of wine, it is s…

0301 basic medicineCancers polyphenolsred wine extractPlateforme de Transfert en Biologie du Cancer (PTBC) ChalminWineCancers Lipids[SHS]Humanities and Social Scienceslymphocyte T Red wine extractchemopreventionLymphocytesEmericMice Inbred BALB CDominiqueInterleukin-17Lymphocyte differentiationVin rougeCell DifferentiationFlavieSanté humaineLipidscolon cancerFemaleInterleukin 17medicine.symptomCancers LimagneColorectal NeoplasmsCancersCancers DelmasBiotechnologyOEnologieInflammationBiology03 medical and health sciencesLymphocytes Tumor-InfiltratingImmune systemCell Line TumorCancers CourtautmedicineAnimalsHumanslymphocytes Th17Cell ProliferationNutrition030109 nutrition & dieteticsFannyPlant ExtractsInterleukinsPolyphenolsHCT116 CellsAntineoplastic Agents PhytogenicXenograft Model Antitumor AssaysMice Inbred C57BL030104 developmental biologyTumor progressionSTAT proteinCancer researchTh17 CellsCytokine secretionVirginieInflammasome complex[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyFood Science
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RBFOX1, encoding a splicing regulator, is a candidate gene for aggressive behavior

2020

The RBFOX1 gene (or A2BP1) encodes a splicing factor important for neuronal development that has been related to autism spectrum disorder and other neurodevelopmental phenotypes. Evidence from complementary sources suggests that this gene contributes to aggressive behavior. Suggestive associations with RBFOX1 have been identified in genome-wide association studies (GWAS) of anger, conduct disorder, and aggressive behavior. Nominal association signals in RBFOX1 were also found in an epigenome-wide association study (EWAS) of aggressive behavior. Also, variants in this gene affect temporal lobe volume, a brain area that is altered in several aggression-related phenotypes. In animals, this gen…

0301 basic medicineCandidate geneNeuroimagingRBFOX1Genome-wide association studyBiologyEpigenesis GeneticA2BP103 medical and health sciencesAll institutes and research themes of the Radboud University Medical Center0302 clinical medicineGeneticsmedicineAnimalsHumansPharmacology (medical)TranscriptomicsRBFOX1Genetic Association StudiesBiological PsychiatryRegulator genePharmacologyGeneticsNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]AggressionGenetic Variationmedicine.diseasePhenotypeAnimal modelsAggressionPsychiatry and Mental health030104 developmental biologyNeurologyAutism spectrum disorderEpigeneticsRBFOX1 GeneRNA Splicing FactorsNeurology (clinical)medicine.symptom030217 neurology & neurosurgeryGenome-Wide Association Study
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