Search results for " Transcription factor"

showing 10 items of 656 documents

Detection of postoperative plasma circulating tumour DNA and lack of CDX2 expression as markers of recurrence in patients with localised colon cancer

2020

BACKGROUND: Colon cancer (CC) is a heterogeneous disease. Novel prognostic factors beyond pathological staging are required to accurately identify patients at higher risk of relapse. Integrating these new biological factors, such as plasma circulating tumour DNA (ctDNA), CDX2 staining, inflammation-associated cytokines and transcriptomic consensus molecular subtypes (CMS) classification, into a multimodal approach may improve our accuracy in determining risk of recurrence.; METHODS: One hundred and fifty patients consecutively diagnosed with localised CC were prospectively enrolled in our study. ctDNA was tracked to detect minimal residual disease by droplet digital PCR. CDX2 expression was…

OncologyCancer Researchmedicine.medical_specialtyColorectal cancerPathological stagingConsensus molecular subtypesPerineural invasionlcsh:RC254-282Circulating Tumor DNAInternal medicinemedicineBiomarkers TumorHumansDigital polymerase chain reactionCDX2 Transcription Factor1506plasma circulating-tumor DNAStage (cooking)Original Researchbusiness.industryInterleukin-6Plasma circulating-tumor DNA.Multimodal therapymedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPrognosisMinimal residual diseaseColon cancerOncologyColonic NeoplasmsCDX2 homeoprotein; colon cancer; consensus molecular subtypes; interleukin-6; plasma circulating-tumor DNANeoplasm Recurrence LocalbusinessCDX2 homeoproteinImmunostaining
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The combined role of biomarkers and interim PET scan in prediction of treatment outcome in classical Hodgkin's lymphoma: a retrospective, European, m…

2016

BACKGROUND: Early-interim fluorodeoxyglucose (FDG)-PET scan after two ABVD (doxorubicin, bleomycin, vinblastine, and dacarbazine) chemotherapy courses (PET-2) represents the most effective predictor of treatment outcome in classical Hodgkin's lymphoma. We aimed to assess the predictive value of PET-2 combined with tissue biomarkers in neoplastic and microenvironmental cells for this disease.METHODS: We enrolled 208 patients with classical Hodgkin's lymphoma and treated with ABVD (training set), from Jan 1, 2002, to Dec 31, 2009, and validated the results in a fully matched independent cohort of 102 patients with classical Hodgkin's lymphoma (validation set), enrolled from Jan 1, 2008, to De…

OncologyMaleDenmarkProgrammed Cell Death 1 ReceptorCohort Studies0302 clinical medicineRecurrenceAntineoplastic Combined Chemotherapy ProtocolsTumor MicroenvironmentMedicineTreatment FailureReed-Sternberg CellsHazard ratioHematologyHodgkin DiseaseVinblastineDacarbazineSTAT1 Transcription FactorItalylymphoma PET Hodgkin030220 oncology & carcinogenesisDisease ProgressionbiomarkerFemalemedicine.drugAdultmedicine.medical_specialtyDacarbazineAntigens Differentiation MyelomonocyticSettore MED/08 - Anatomia PatologicaVinblastineDisease-Free Survival03 medical and health sciencesBleomycinAntigens CDInternal medicineHumansRetrospective StudiesFluorodeoxyglucosebusiness.industryRetrospective cohort studyPET scanmedicine.diseaseLymphomaSurgeryABVDReed–Sternberg cellDoxorubicinPositron-Emission TomographyMultivariate Analysisclassical Hodgkin's lymphoma:PolandbusinessBiomarkers030215 immunology
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NUPR1 works against the metabolic stress-induced autophagy-associated cell death in pancreatic cancer cells.

2013

The incidence of pancreatic adenocarcinoma is increasing with more than 43,000 predicted new cases in the US and 65,000 in Europe this year. Pancreatic cancer patients have a short life expectancy with less than 3–4% 5-y survival, which results in an equivalent incidence and mortality rate. One of the major challenges in pancreatic cancer is the identification of pharmacological approaches that overcome the resistance of this cancer to therapy. Intensive research in the past decades has led to the classification of pancreatic cancers and the identification of the driver key genetic events. Despite the advances in understanding the molecular mechanisms responsible for pancreatic cancer patho…

Oncologymedicine.medical_specialtyCell SurvivalDrug resistanceDiseaseBiologyProtein Serine-Threonine KinasesModels BiologicalAurora KinasesStress PhysiologicalPancreatic cancerInternal medicineCarcinomamedicineAutophagyBasic Helix-Loop-Helix Transcription FactorsHumansMolecular BiologyCell DeathMechanism (biology)Mortality rateCancerCell Biologymedicine.diseaseAutophagic PunctumNeoplasm ProteinsEndocrinologyDrug Resistance NeoplasmAdenocarcinomaCarcinoma Pancreatic DuctalAutophagy
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Survivin is regulated by interleukin-4 in colon cancer stem cells

2010

Colorectal cancer has provided an important model to test the stem cell hypothesis of cancer origin, which implies that cancer arises as a result of genetic aberrations in stem cells leading to deregulation of the proliferation/differentiation balance. We and others have demonstrated that, similarly to other solid tumors, colon carcinogenesis and progression are dictated by highly apoptosis-resistant stem-like cells. Our data have suggested that protection from apoptosis is achieved by autocrine production of interleukin-4 (IL-4) through up-regulation of anti-apoptotic mediators. In this study, we extend our analysis to another apoptosis inhibitor widely expressed in tumors, namely survivin…

Organoplatinum CompoundsPhysiologyColorectal cancerSurvivinmedicine.medical_treatmentClinical BiochemistryFluorescent Antibody TechniqueAntineoplastic AgentsApoptosisBiologyInhibitor of Apoptosis ProteinsSurvivin inetrleukin-4Cancer stem cellSurvivinIn Situ Nick-End LabelingmedicineHumansPhosphorylationAutocrine signallingInterleukin 4Staining and LabelingCancerIsoxazolesCell Biologymedicine.diseaseGene Expression Regulation NeoplasticOxaliplatinProtein TransportCytokineImmunologyNeoplastic Stem CellsCancer researchInterleukin-4Stem cellColorectal NeoplasmsSTAT6 Transcription FactorMicrotubule-Associated ProteinsLeflunomideJournal of Cellular Physiology
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The transcription factor IRF1 dictates the IL-21-dependent anticancer functions of TH9 cells

2014

The TH9 subset of helper T cells was initially shown to contribute to the induction of autoimmune and allergic diseases, but subsequent evidence has suggested that these cells also exert antitumor activities. However, the molecular events that account for their effector properties are elusive. Here we found that the transcription factor IRF1 enhanced the effector function of TH9 cells and dictated their anticancer properties. Under TH9-skewing conditions, interleukin 1β (IL-1β) induced phosphorylation of the transcription factor STAT1 and subsequent expression of IRF1, which bound to the promoters of Il9 and Il21 and enhanced secretion of the cytokines IL-9 and IL-21 from TH9 cells. Further…

OvalbuminGreen Fluorescent ProteinsImmunologyMelanoma ExperimentalProto-Oncogene Proteins c-fyn3T3 cellsCell LineInterferon-gammaMicemedicineAnimalsImmunology and AllergySTAT1PhosphorylationRNA Small InterferingSTAT4Transcription factorInterleukin 3Mice KnockoutBase SequencebiologySequence Analysis RNAChemistryEffectorInterleukinsInterleukin-9Promoter3T3 CellsT-Lymphocytes Helper-InducerInterleukin-10Cell biologyMice Inbred C57BLSTAT1 Transcription Factormedicine.anatomical_structureCell culturebiology.proteinFemaleRNA InterferenceInterferon Regulatory Factor-1Nature Immunology
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Common variants conferring risk of schizophrenia

2009

Schizophrenia is a complex disorder, caused by both genetic and environmental factors and their interactions. Research on pathogenesis has traditionally focused on neurotransmitter systems in the brain, particularly those involving dopamine. Schizophrenia has been considered a separate disease for over a century, but in the absence of clear biological markers, diagnosis has historically been based on signs and symptoms. A fundamental message emerging from genome-wide association studies of copy number variations (CNVs) associated with the disease is that its genetic basis does not necessarily conform to classical nosological disease boundaries. Certain CNVs confer not only high relative ris…

Pair 6/geneticsGenetics and epigenetic pathways of disease [NCMLS 6]Genome-wide association studyAetiology screening and detection [ONCOL 5]1Q21.1Major Histocompatibility Complex/geneticsMajor Histocompatibility ComplexTranscription Factor 40302 clinical medicineChemicals And Cas Registry NumbersPerception and Action [DCN 1]Copy-number variationPOPULATIONGeneticsPair 18/genetics0303 health scienceseducation.field_of_studyGenomeHuman/geneticsMultidisciplinaryBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsSchizophrenia/*genetics/immunologyGenetic Predisposition to Disease/*genetics3. Good healthDNA-Binding ProteinsNeurogranin/geneticsDISEASESChromosomes Human Pair 6Single Nucleotide/*geneticsFunctional Neurogenomics [DCN 2]Zinc finger protein 804AHumanGenetic MarkersPsychosisGenotypePopulationTranscription Factors/geneticsSingle-nucleotide polymorphismBiologyPolymorphism Single NucleotideChromosomesPair 11/geneticsArticleChromosomes; Human; Pair 11/genetics; Pair 18/genetics; Pair 6/genetics; DNA-Binding Proteins/genetics; Genetic Markers/genetics; Genetic Predisposition to Disease/*genetics; Genome; Human/genetics; Genome-Wide Association Study; Genotype; Humans; Major Histocompatibility Complex/genetics; Neurogranin/genetics; Polymorphism; Single Nucleotide/*genetics; Schizophrenia/*genetics/immunology; Transcription Factors/geneticsGenomic disorders and inherited multi-system disorders [IGMD 3]Molecular epidemiology [NCEBP 1]03 medical and health sciencesTranslational research [ONCOL 3]medicineHumansSNPGenetic Predisposition to DiseasePolymorphismGENOME-WIDE ASSOCIATIONeducation030304 developmental biologyGenetic associationGenetic Markers/geneticsHereditary cancer and cancer-related syndromes [ONCOL 1]Genome HumanChromosomes Human Pair 11MEMORYmedicine.diseaseGENENEUROGRANINDELETIONSSchizophreniabiology.proteinNeurograninChromosomes Human Pair 18DNA-Binding Proteins/geneticsMENTAL-RETARDATIONSCAN030217 neurology & neurosurgeryGenome-Wide Association StudyTranscription Factors
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Endothelial Wnt/β-catenin signaling inhibits glioma angiogenesis and normalizes tumor blood vessels by inducing PDGF-B expression

2012

Wnt modulates glioma vascularization by regulating PDGF-B expression.

PathologyAngiogenesisCentral Nervous System NeoplasmsMice0302 clinical medicineImmunology and AllergyWnt Signaling Pathwaybeta Catenin0303 health sciencesbiologyNeovascularization PathologicBrain NeoplasmsWnt signaling pathwayIntracellular Signaling Peptides and ProteinsForkhead Transcription FactorsGliomaProto-Oncogene Proteins c-sis3. Good healthmedicine.anatomical_structureBlood-Brain Barrier030220 oncology & carcinogenesiscardiovascular systemIntercellular Signaling Peptides and ProteinsFemalemedicine.medical_specialtyBeta-cateninEndotheliumImmunologyNotch signaling pathwayMice NudeWnt1 ProteinMural cellArticle03 medical and health sciencesGliomamedicineAnimalsHumansddc:610neoplasms030304 developmental biologyAdaptor Proteins Signal TransducingCalcium-Binding ProteinsMembrane Proteinsmedicine.diseaseXenograft Model Antitumor Assaysnervous system diseasesDKK1Cancer researchbiology.proteinEndothelium VascularNeoplasm Grading
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IL-22 is produced by innate lymphoid cells and limits inflammation in allergic airway disease

2011

Interleukin (IL)-22 is an effector cytokine, which acts primarily on epithelial cells in the skin, gut, liver and lung. Both pro- and anti-inflammatory properties have been reported for IL-22 depending on the tissue and disease model. In a murine model of allergic airway inflammation, we found that IL-22 is predominantly produced by innate lymphoid cells in the inflamed lungs, rather than TH cells. To determine the impact of IL-22 on airway inflammation, we used allergen-sensitized IL-22-deficient mice and found that they suffer from significantly higher airway hyperreactivity upon airway challenge. IL-22-deficiency led to increased eosinophil infiltration lymphocyte invasion and production…

PathologyPulmonologymedicine.medical_treatmentT-LymphocytesIntracellular Spacelcsh:Medicine10263 Institute of Experimental ImmunologyInterleukin 22Mice0302 clinical medicineLymphocytesPhosphorylationlcsh:ScienceLung0303 health sciencesMultidisciplinaryInterleukin-13T CellsAllergy and HypersensitivityInnate lymphoid cellInterleukinrespiratory systemInnate ImmunityRecombinant Proteins3. Good healthCytokinemedicine.anatomical_structureInterleukin 13CytokinesMedicineTumor necrosis factor alphaBiological Markersmedicine.symptomResearch ArticleSTAT3 Transcription Factormedicine.medical_specialtyImmune CellsImmunologyAntigen-Presenting CellsImmunoglobulinsInflammation610 Medicine & health1100 General Agricultural and Biological SciencesBiology03 medical and health sciences1300 General Biochemistry Genetics and Molecular BiologymedicineRespiratory HypersensitivityAnimalsBiology030304 developmental biologyInflammation1000 MultidisciplinaryTumor Necrosis Factor-alphaInterleukinslcsh:RImmunityEpithelial CellsEosinophilAllergensAsthmaImmunity Innaterespiratory tract diseasesImmune SystemImmunology570 Life sciences; biologylcsh:QImmunizationBiomarkers030215 immunology
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Notch signalling is off and is uncoupled from HES1 expression in Ewing's sarcoma

2010

Notch can act as an oncogene or as a tumour suppressor and thus can either promote or inhibit tumour cell growth. To establish Notch status in Ewing's sarcoma family of tumours (ESFT), we investigated the Notch pathway by gene expression profiling meta-analysis or immunohistochemistry in samples obtained from 96 and 24 ESFT patients, respectively. We found that although Notch receptors were highly expressed, Notch did not appear to be active, as evidenced by the absence of Notch receptors in cell nuclei. In contrast, we show that Notch receptors known to be active in colon adenocarcinoma, hepatocarcinoma, and pancreatic carcinoma stain cell nuclei in these tumours. High expression of the No…

Pathologymedicine.medical_specialtyCellNotch signaling pathwayBone NeoplasmsSarcoma EwingBiologyPathology and Forensic MedicineBasic Helix-Loop-Helix Transcription FactorsTumor Cells CulturedmedicineHumansHES1HEY1Transcription factorCell ProliferationCell NucleusHomeodomain ProteinsRegulation of gene expressionReceptors NotchCell growthGene Expression ProfilingNeoplasm ProteinsGene Expression Regulation Neoplasticmedicine.anatomical_structureNeoplastic Stem CellsCancer researchTranscription Factor HES-1Cyclin-dependent kinase 8Signal TransductionThe Journal of Pathology
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Immunohistochemical study of correlation between histologic subtype and expression of epithelial-mesenchymal transition-related proteins in synovial …

2011

Context.—Synovial sarcomas are mesenchymal tumors with epithelial nature and comprise biphasic and monophasic fibrous subtypes. However, factors determining epithelial or spindle cell differentiation are still unexplored. Aberrant epithelial-mesenchymal transition has been implicated in the pathogenesis of diverse human malignancies.Objective.—To analyze the correlation between cellular phenotype and expression of proteins associated with different epithelial-mesenchymal transition-related pathways.Design.—Immunohistochemical analysis of E-cadherin, Snail, Slug, and dysadherin, components of the Wnt/wingless and PI3K/Akt pathways, was performed on 14 biphasic and 27 monophasic fibrous tumor…

Pathologymedicine.medical_specialtyEpithelial-Mesenchymal TransitionCellBiologyIon ChannelsPathology and Forensic MedicineSarcoma SynovialmedicineBiomarkers TumorHumansEpithelial–mesenchymal transitionMembrane GlycoproteinsMesenchymal stem cellMicrofilament ProteinsGeneral Medicinemedicine.diseaseCadherinsImmunohistochemistryNeoplasm ProteinsMedical Laboratory Technologymedicine.anatomical_structureTissue Array AnalysisSnail Family Transcription FactorsImmunohistochemistrySarcomaSnail Family Transcription FactorsTranscription FactorsArchives of pathologylaboratory medicine
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