Search results for "82"

showing 10 items of 2220 documents

Targeting BRAF and RAS in Colorectal Cancer

2021

Simple Summary In colorectal cancer, mutations of the KRAS and BRAF genes are quite common and can contribute to the activation of cell signaling pathways that lead to cell proliferation and differentiation. These processes promote cancer growth, and in some cases, they may cause cells to develop resistance to certain types of treatment, notably EGFR inhibitors. We summarize recent knowledge regarding the effects of KRAS and BRAF mutations in the setting of colorectal cancer and discuss the new therapies under development. Abstract Colorectal cancer (CRC) is still one of the most frequent forms of cancer in the world in terms of incidence. Around 40% of CRC patients carry a mutation of the …

0301 basic medicineMAPK/ERK pathwayCancer ResearchColorectal cancerAngiogenesismedicine.medical_treatmentcolorectal cancerReviewmedicine.disease_causeBRAFTargeted therapy03 medical and health sciences0302 clinical medicineKRASmedicineneoplasmsRC254-282EGFR inhibitorsMutationbusiness.industryNeoplasms. Tumors. Oncology. Including cancer and carcinogensCancertargeted therapymedicine.diseasedigestive system diseases030104 developmental biologyOncology030220 oncology & carcinogenesisCancer researchKRASbusinessCancers
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Ellagitannin-rich cloudberry inhibits hepatocyte growth factorinduced cell migration and phosphatidylinositol 3-kinase/AKT activation in colon carcin…

2016

// Anne-Maria Pajari 1, 2 , Essi Paivarinta 1 , Lassi Paavolainen 3 , Elina Vaara 1 , Tuuli Koivumaki 4 , Ritu Garg 5 , Anu Heiman-Lindh 1 , Marja Mutanen 1 , Varpu Marjomaki 3 , Anne J. Ridley 2, 5 1 Department of Food and Environmental Sciences, Division of Nutrition, University of Helsinki, Helsinki, Finland 2 University College London, Ludwig Institute for Cancer Research, London, UK 3 Department of Biological and Environmental Science / Nanoscience Center, University of Jyvaskyla, Jyvaskyla, Finland 4 Department of Food and Environmental Sciences, Division of Food Chemistry, University of Helsinki, Helsinki, Finland 5 Randall Division of Cell & Molecular Biophysics, King’s College Lond…

0301 basic medicineMAPK/ERK pathwaycell migrationColorectal cancerCellMetastasisMicePhosphatidylinositol 3-Kinases0302 clinical medicineCell MovementHepatocyte Growth FactorHydrolyzable Tanninsmedicine.anatomical_structureOncology030220 oncology & carcinogenesisColonic NeoplasmsHepatocyte growth factormedicine.drugResearch PapersolumigraatioAntineoplastic Agentscolorectal cancerMet receptorAdenocarcinoma03 medical and health sciencesCell Line TumorellagitanninsmedicineJournal ArticleAnimalsHumansCell migrationProtein kinase Bbusiness.industryPlant Extractsta1182Cancerta3122medicine.diseaseMice Mutant StrainsMin mouseEnzyme ActivationMice Inbred C57BL030104 developmental biologyCancer cellImmunologyCancer researchbusinessRubusProto-Oncogene Proteins c-akt
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Negatively Charged Gangliosides Promote Membrane Association of Amphipathic Neurotransmitters

2018

Lipophilic neurotransmitters (NTs) such as dopamine are chemical messengers enabling neurotransmission by adhering onto the extracellular surface of the post-synaptic membrane in a synapse, followed by binding to their receptors. Previous studies have shown that the strength of the NT-membrane association is dependent on the lipid composition of the membrane. Negatively charged lipids such as phosphatidylserine, phosphatidylglycerol, and phosphatidic acid have been indicated to promote NT-membrane binding, however these anionic lipids reside almost exclusively in the intracellular leaflet of the post-synaptic membrane instead of the extracellular leaflet facing the synaptic cleft. Meanwhile…

0301 basic medicineMOLECULAR-DYNAMICS SIMULATIONSBIOMOLECULAR SYSTEMSkolesteroliasetyylikoliiniSynaptic TransmissionsolukalvotCell membranechemistry.chemical_compoundSCHIZOPHRENIAmolekyylidynamiikkamolecular dynamics (MD)neurotransmissionvälittäjäaineetChemistryLIPID-MEMBRANESGeneral NeurosciencePhosphatidylserineALZHEIMERS-DISEASEMembranemedicine.anatomical_structureHAMILTONIAN REPLICA EXCHANGElipids (amino acids peptides and proteins)dopamineIntracellularneurotransmittermonosialotetrahexosylganglioside (GM1)Synaptic cleftG(M1) GangliosideMolecular Dynamics SimulationNeurotransmission03 medical and health sciencesExtracellularmedicineAnimalsmonosialotetrahexosylgangliosidebinding free energyPhosphatidylglyceroldopamiiniBinding SitesCell Membranehistamiini3112 Neurosciencesta1182cholesterolBILAYERhistamineacetylcholinehermosolut030104 developmental biologyFORCE-FIELDBiophysicssynapsit
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Somatic copy number alterations are associated with EGFR amplification and shortened survival in patients with primary glioblastoma.

2019

Glioblastoma (GBM) is the most common malignant primary tumor of the central nervous system. With no effective therapy, the prognosis for patients is terrible poor. It is highly heterogeneous and EGFR amplification is its most frequent molecular alteration. In this light, we aimed to examine the genetic heterogeneity of GBM and to correlate it with the clinical characteristics of the patients. For that purpose, we analyzed the status of EGFR and the somatic copy number alterations (CNAs) of a set of tumor suppressor genes and oncogenes. Thus, we found GBMs with high level of EGFR amplification, low level and with no EGFR amplification. Highly amplified tumors showed histological features of…

0301 basic medicineMaleCancer ResearchBiopsyL-amp GB EGFR-low amplified glioblastomamedicine.disease_causewt wildtypeMYBPC3 myosin-binding protein C0302 clinical medicineHIC1 hypermethylated in cancer 1Gene duplicationIn Situ Hybridization FluorescenceIDH2 isocitrate dehydrogenase 2MutationRB-pat RB signaling pathwayEGFRvIII epidermal growth factor receptor variant number IIIPAH phenylalanine hydroxylaseGBM glioblastoma IDH-wildtype (glioblastoma multiforme primary glioblastoma).ANOVA ANalysis Of VArianceN-amp GB EGFR-no amplified glioblastomaMiddle AgedCDKN2A cyclin-dependent kinase inhibitor 2Alcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPrognosisPrimary tumorImmunohistochemistryH-amp GB EGFR-high amplified glioblastomaErbB ReceptorsTKR-pat tyrosine-kinase receptors signaling pathway030220 oncology & carcinogenesisDisease ProgressionCDK6 cyclin-dependent kinase 6CDH1 Cadherin 1FemaleCREM cAMP response element modulatorIHC immunohistochemistryAdultOriginal articleDNA Copy Number VariationsCDKN1B cyclin-dependent kinase inhibitor 1BBiologyRARB retinoic acid receptor betaCNS central nervous systemlcsh:RC254-282IDH1 isocitrate dehydrogenase 1BCL2 B-cell cll/ lymphoma 2CNAs copy number algerationsWHO World Health Organization03 medical and health sciencesYoung Adultp53-pat p53 signaling pathwaymedicineBiomarkers TumorTMA tissue microarrayPTENHumansProtein kinase BPI3K/AKT/mTOR pathwaySurvival analysisAgedGenetic heterogeneityGene AmplificationGFAP glial fibrillary acidic proteinMLPA multiplex ligation-dependent probe amplificationmedicine.diseaseFISH fluorescence in situ hibridizationSurvival AnalysisCDKN2B cyclin-dependent kinase inhibitor 2BPTEN phosphatase and tensin homologEGFR epidermal growth factor receptorCNV-load load of copy number variations030104 developmental biologyMutationPARK2 parkinCancer researchbiology.proteinTCGA The Cancer Genome AtlasLARGE1 acetylglucosaminyltransferase-like protein 1GlioblastomaCHD7 Chromodomain Helicase DNA Binding Protein 7DAPI 4′6-diamidino-2-phenylindoleNeoplasia (New York, N.Y.)
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Intratumoral immunosuppression profiles in 11q-deleted neuroblastomas provide new potential therapeutic targets

2021

In this issue, Coronado et al. attempt to improve our understanding of the factors affecting the response to immunotherapy in a large subset of high‐risk neuroblastoma with hemizygous deletion of chromosome 11q. By using several computational approaches, the authors study potential transcriptional and post‐transcriptional pathways that may affect the response to immunotherapy and further be leveraged therapeutically in a biomarker‐directed fashion.

0301 basic medicineMaleCancer Researchmedicine.medical_treatmentRetinoic acidchemistry.chemical_compoundNeuroblastoma0302 clinical medicineTumor Microenvironment11q deletion anti-GD2 immunotherapy combination immunotherapy immune cell infiltration miRNAs neuroblastomaMedicineeducation.field_of_studyimmune cell infiltration11q deletionImmunosuppressionGeneral Medicinelcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPatologiaNeoplasm ProteinsmicroRNAsSurvival Rateanti‐GD2 therapyOncology030220 oncology & carcinogenesiscombination immunotherapymiRNAsMolecular Medicineimmune checkpoint inhibitionFemaleImmunotherapyChromosome Deletionanti‐GD2 immunotherapyPopulationlcsh:RC254-282Disease-Free Survival03 medical and health sciencesImmune systemNeuroblastomaGeneticsImmune ToleranceHumanseducationRetrospective Studiesbusiness.industryChromosomes Human Pair 11Immunotherapymedicine.diseaseImmune checkpointBlockade030104 developmental biologychemistryCancer researchCommentarybusiness
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Δ133p53α enhances metabolic and cellular fitness of TCR-engineered T cells and promotes superior antitumor immunity

2021

BackgroundTumor microenvironment-associated T cell senescence is a key limiting factor for durable effective cancer immunotherapy. A few studies have demonstrated the critical role of the tumor suppressor TP53-derived p53 isoforms in cellular senescence process of non-immune cells. However, their role in lymphocytes, in particular tumor-antigen (TA) specific T cells remain largely unexplored.MethodsHuman T cells from peripheral blood were retrovirally engineered to coexpress a TA-specific T cell receptor and the Δ133p53α-isoform, and characterized for their cellular phenotype, metabolic profile and effector functions.ResultsPhenotypic analysis of Δ133p53α-modified T cells revealed a marked …

0301 basic medicineMaleCancer Researchmedicine.medical_treatmentT cellT-LymphocytesImmunologyReceptors Antigen T-Cell2436receptorsBiologycell engineeringadoptive03 medical and health sciencesMice0302 clinical medicineantigenTIGITCancer immunotherapyAntigenCell Line TumorNeoplasmsmedicineTumor MicroenvironmentImmunology and AllergyAnimalsHumans1506RC254-282PharmacologyImmune Cell Therapies and Immune Cell EngineeringCD28Neoplasms. Tumors. Oncology. Including cancer and carcinogensT lymphocyteImmunotherapycostimulatory and inhibitory T-cell receptorsCell biology030104 developmental biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesisMolecular MedicineimmunotherapyCD8Journal for ImmunoTherapy of Cancer
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Prolonged sleep restriction induces changes in pathways involved in cholesterol metabolism and inflammatory responses

2016

Article

0301 basic medicineMaleEpidemiologyPhysiologychemistry.chemical_compoundinsufficient sleep0302 clinical medicineHigh-density lipoproteinFinlandSleep restrictionGENERAL-POPULATIONINSULIN-RESISTANCEeducation.field_of_studyMultidisciplinarytulehdusCARDIOVASCULAR RISKGLUCOSE-METABOLISMta3142Chronic inflammationMiddle AgedSleep in non-human animals3. Good healthSleep deprivationCholesterolMetabolomeFemalemedicine.symptomAdultmedicine.medical_specialtyACUTE-PHASE RESPONSELIVER-X-RECEPTORSPopulationBiologyta3111Articlesleep restriction03 medical and health sciencesInsulin resistanceMetabolic DiseasesInternal medicinemedicineMetabolomeHumansCORONARY-HEART-DISEASEeducationLiver X receptorDyslipidaemiasAgedCASSETTE TRANSPORTER G1Gene Expression Profilingta1182ta3121medicine.diseaseSleep deprivation030104 developmental biologyEndocrinologychemistryinflammationcholesterol metabolismSleep Deprivation3111 BiomedicineGene expressionHIGH-DENSITY-LIPOPROTEIN030217 neurology & neurosurgeryBlood Chemical AnalysisScientific Reports
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Maternal Inheritance of a Recessive RBP4 Defect in Canine Congenital Eye Disease

2018

SUMMARY Maternally skewed transmission of traits has been associated with genomic imprinting and oocyte-derived mRNA. We report canine congenital eye malformations, caused by an amino acid deletion (K12del) near the N terminus of retinol-binding protein (RBP4). The disease is only expressed when both dam and offspring are deletion homozygotes. RBP carries vitamin A (retinol) from hepatic stores to peripheral tissues, including the placenta and developing eye, where it is required to synthesize retinoic acid. Gestational vitamin A deficiency is a known risk factor for ocular birth defects. The K12del mutation disrupts RBP folding in vivo, decreasing its secretion from hepatocytes to serum. T…

0301 basic medicineMaleNon-Mendelian inheritanceProtein Foldingcongenital eye defectEye Diseasesgenetic structuresNATIVE DISULFIDE BONDSMedical PhysiologyRetinoic acidReproductive health and childbirth413 Veterinary scienceMicrophthalmiavitamin Achemistry.chemical_compoundPlasmaA-vitamiini2.1 Biological and endogenous factorsMicrophthalmosPrealbuminCRYSTAL-STRUCTUREAetiologyBase Pairinglcsh:QH301-705.5Sequence DeletionPediatricwhole genome sequencingVITAMIN-A-DEFICIENCYANOPHTHALMIAPenetrancePedigreemedicine.anatomical_structurePhenotypeFemalemedicine.medical_specialtyGenotypeENDOPLASMIC-RETICULUMGenes RecessiveMETABOLISMBiologyGeneral Biochemistry Genetics and Molecular BiologyArticle03 medical and health sciencesDogscanine geneticsInternal medicinePlacentaRETINOL-BINDING-PROTEINGeneticsmedicineAnimalsHumansRecessiveMALFORMATIONSBIOCHEMICAL BASISAmino Acid SequenceAlleleEye Disease and Disorders of VisionNutritiongenome-wide association study030102 biochemistry & molecular biologywestern blottingMUTATIONSta1184RBP4maternal inheritancemedicine.diseaseRetinol-Binding ProteinsRetinol binding proteinnuclear magnetic resonance030104 developmental biologyEndocrinologychemistryGeneslcsh:Biology (General)microphthalmiaGenetic LociHela Cells1182 Biochemistry cell and molecular biologyCongenital Structural Anomalies3111 BiomedicineBiochemistry and Cell BiologyDigestive DiseasesGenomic imprintingRetinol-Binding Proteins PlasmaHeLa Cells
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Microenvironment in neuroblastoma: isolation and characterization of tumor-derived mesenchymal stromal cells

2018

Background It has been proposed that mesenchymal stromal cells (MSCs) promote tumor progression by interacting with tumor cells and other stroma cells in the complex network of the tumor microenvironment. We characterized MSCs isolated and expanded from tumor tissues of pediatric patients diagnosed with neuroblastomas (NB-MSCs) to define interactions with the tumor microenvironment. Methods Specimens were obtained from 7 pediatric patients diagnosed with neuroblastoma (NB). Morphology, immunophenotype, differentiation capacity, proliferative growth, expression of stemness and neural differentiation markers were evaluated. Moreover, the ability of cells to modulate the immune response, i.e. …

0301 basic medicineMaleRegistrieCancer ResearchCellular differentiationMesenchymal stromal cellsCell SeparationNeuroblastoma0302 clinical medicineImmunophenotypingCancer-Associated FibroblastsTumor MicroenvironmentCytotoxic T cellRegistriesStemnessCancer-Associated FibroblastCoculture TechniqueChildrenCells CulturedStemneChemistryMesenchymal stromal cellCell CycleEMTCell Differentiationlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensImmunohistochemistryMesenchymal Stem CellOncology030220 oncology & carcinogenesisChild PreschoolPopulation SurveillanceBone Marrow CellFemaleResearch ArticleHumanSignal TransductionStromal cellMicroenvironmentBone Marrow Cellslcsh:RC254-282Immunophenotyping03 medical and health sciencesGeneticsBiomarkers TumorHumansSettore MED/04 - Patologia GeneraleTumor microenvironmentGene Expression ProfilingMesenchymal stem cellInfantMesenchymal Stem CellsCoculture Techniques030104 developmental biologyTumor progressionCancer cellMutationCancer research
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Dopaminergic-GABAergic interplay and alcohol binge drinking

2019

© 2019 Elsevier Ltd The dopamine D 3 receptor (D 3 R), in the nucleus accumbens (NAc), plays an important role in alcohol reward mechanisms. The major neuronal type within the NAc is the GABAergic medium spiny neuron (MSN), whose activity is regulated by dopaminergic inputs. We previously reported that genetic deletion or pharmacological blockade of D 3 R increases GABA A α6 subunit in the ventral striatum. Here we tested the hypothesis that D 3 R-dependent changes in GABA A α6 subunit in the NAc affect voluntary alcohol intake, by influencing the inhibitory transmission of MSNs. We performed in vivo and ex vivo experiments in D 3 R knockout (D 3 R −/− ) mice and wild type littermates (D 3 …

0301 basic medicineMalemedicine.medical_specialtyDopaminergic-GABAergicSettore BIO/09 - FISIOLOGIAAlpha6 subunit; Dopamine D3 receptor; Ethanol; Furosemide (PubChem CID: 3440); GABA(A)receptor; Nucleus accumbens; Ro 15-4513; Ro 15-4513 (PubChem CID: 5081); SB 277011A (PubChem CID: 75358288)Alpha6 subunitNucleus accumbensMedium spiny neuronInhibitory postsynaptic potentialNucleus AccumbensBinge Drinking03 medical and health sciencesMiceDopamine D3 receptor0302 clinical medicineDopamine receptor D3Internal medicinemedicineAnimalsFurosemide (PubChem CID: 3440)Nucleus accumbenPharmacology & PharmacyRNA MessengerRo 15-4513GABAergic NeuronsSB 277011A (PubChem CID: 75358288).PharmacologyMice KnockoutEthanolGABAA receptorChemistryDopaminergicAntagonistReceptors Dopamine D3Receptors GABA-ARo 15-4513 (PubChem CID: 5081)GABA(A)receptor3. Good healthProtein Subunits030104 developmental biologyEndocrinologynervous systemGene Expression Regulation030220 oncology & carcinogenesisGABAergicNucleus accumbensSB 277011A (PubChem CID: 75358288)
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