Search results for "Myc"

showing 10 items of 3773 documents

The mycotoxin zearalenone enhances cell proliferation, colony formation and promotes cell migration in the human colon carcinoma cell line HCT116.

2016

IF 3.522; International audience; Zearalenone (ZEN) and Aflatoxin B1 (AFB1) are fungal secondary metabolites produced by Fusarium and Aspergillus genera, respectively. These mycotoxins are found world-wide as corn and wheat contaminants. AFB1 is probably the most toxic and carcinogenic mycotoxin. It has been demonstrated to be mutagenic, genotoxic, and hepatocarcinogenic. ZEN is a non-steroidal estrogenic mycotoxin that displays hepatotoxicity, immunotoxicity and genotoxicity. Its mutagenic and carcinogenic properties have so far remained controversial and questionable. Using the colon carcinoma cell line HCT116, we will show here that ZEN, at low concentrations, enhances cell proliferation…

0301 basic medicineBone-Marrow-CellsAflatoxinAflatoxin B1Time Factors[ SDV.TOX ] Life Sciences [q-bio]/ToxicologyToxicologymedicine.disease_causeInductionchemistry.chemical_compound0302 clinical medicineProliferation assayCell MovementZearalenonebiologyfood and beveragesCell migrationGeneral MedicineMigration assayDna-Damage030220 oncology & carcinogenesis[SDV.TOX]Life Sciences [q-bio]/ToxicologyColonic NeoplasmsZearalenoneChromosome-AberrationsBalb/C MiceFusariumendocrine systemPreventive Role03 medical and health sciencesBotanymedicineHumansNeoplasm InvasivenessMycotoxinCarcinogenCell ProliferationWound HealingDose-Response Relationship DrugCell growthfungiClonogenic assaybiology.organism_classificationHCT116 CellsMolecular biology030104 developmental biologychemistryMcf-7 CellsFusarium ToxinsIn-VitroVitamin-ECarcinogensGenotoxicityToxicology letters
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Gut Microbiota Condition the Therapeutic Efficacy of Trastuzumab in HER2-Positive Breast Cancer.

2021

Abstract Emerging evidence indicates that gut microbiota affect the response to anticancer therapies by modulating the host immune system. In this study, we investigated the impact of gut microbiota on immune-mediated trastuzumab antitumor efficacy in preclinical models of HER2-positive breast cancer and in 24 patients with primary HER2-positive breast cancer undergoing trastuzumab-containing neoadjuvant treatment. In mice, the antitumor activity of trastuzumab was impaired by antibiotic administration or fecal microbiota transplantation from antibiotic-treated donors. Modulation of the intestinal microbiota was reflected in tumors by impaired recruitment of CD4+ T cells and granzyme B–posi…

0301 basic medicineCD4-Positive T-LymphocytesCancer ResearchReceptor ErbB-2medicine.medical_treatmentGut floraGranzymesMice0302 clinical medicineAntineoplastic Agents ImmunologicalTrastuzumabTumor Microenvironmentskin and connective tissue diseasesNeoadjuvant therapybiologyFecal Microbiota TransplantationInterleukin-12Neoadjuvant TherapyAnti-Bacterial AgentsTreatment OutcomeOncology030220 oncology & carcinogenesisStreptomycinCytokinesGut microbiota trastuzumab breast cancerFemaleTaxoidsmedicine.drugBridged-Ring CompoundsBreast NeoplasmsSettore MED/08 - Anatomia PatologicaNitric Oxide03 medical and health sciencesImmune systemBreast cancerVancomycinmedicineAnimalsHumansCyclophosphamideImmunity Mucosalbusiness.industryLachnospiraceaeDendritic cellDendritic CellsTrastuzumabbiology.organism_classificationmedicine.diseaseGastrointestinal Microbiome030104 developmental biologyGranzymeDoxorubicinImmune Systembiology.proteinCancer researchInterferonsbusinessCancer research
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Prediabetes is associated with the modulation of antigen-specific Th1/Tc1 and Th17/Tc17 responses in latent Mycobacterium tuberculosis infection.

2017

Type 2 diabetes mellitus (DM) is associated with the down modulation of Th1, Th2 and Th17 responses in latent Mycobacterium tuberculosis infection but the role of prediabetes (PDM) in this setting is not well understood. To examine the role of CD4+ and CD8+ T cell cytokines in latent tuberculosis (LTB) with coincident PDM, we studied the baseline, mycobacterial, control antigen and mitogen-stimulated T cell cytokine responses in LTB individuals with (LTB-PDM; n = 20) or without (LTB-NDM; n = 20) concomitant prediabetes. LTB-PDM is characterized by diminished frequencies of mono-and dual-functional CD4+ Th1 and Th17 cells and mono-functional Th2 cells at baseline and/or following mycobacteri…

0301 basic medicineCD4-Positive T-LymphocytesMaleBacterial DiseasesPhysiologymedicine.medical_treatmentlcsh:MedicineCD8-Positive T-LymphocytesWhite Blood Cells0302 clinical medicineSpectrum Analysis TechniquesEndocrinologyAnimal CellsImmune PhysiologyMedicine and Health SciencesMedicinePrediabeteslcsh:ScienceInnate Immune SystemMultidisciplinarybiologyLatent tuberculosisT CellsMiddle AgedFlow Cytometry3. Good healthActinobacteriaCytokinemedicine.anatomical_structureInfectious DiseasesSpectrophotometryCytokinesFemaleCytophotometryCellular TypesResearch ArticleAdultEndocrine DisordersT cellImmune CellsImmunologyCytotoxic T cellsResearch and Analysis MethodsMycobacterium tuberculosisPrediabetic State03 medical and health sciencesImmune systemTh2 CellsAntigenLatent TuberculosisDiabetes MellitusHumansTuberculosisT Helper CellsAgedAntigens BacterialBlood CellsBacteriabusiness.industrylcsh:ROrganismsBiology and Life SciencesMycobacterium tuberculosisCell BiologyTh1 CellsMolecular Developmentmedicine.diseasebiology.organism_classificationTropical Diseases030104 developmental biologyCase-Control StudiesImmune SystemMetabolic DisordersImmunologyTh17 Cellslcsh:QbusinessCD8030215 immunologyDevelopmental BiologyPloS one
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Increased expression of interleukin-22 in patients with giant cell arteritis

2017

Objectives GCA is characterized by arterial remodelling driven by inflammation. IL-22 is an attractive cytokine which acts at the crosstalk between immune and stromal cells. We hypothesized that IL-22 might be induced in GCA and might be involved in disease pathogenesis. Methods Patients subjected to temporal artery biopsies (TABs) naive from therapy were enrolled: 27 biopsy-proven GCA, 8 biopsy-negative GCA, 21 biopsy-negative non-GCA patients. Expression of IL-22 was determined in TABs by immunohystochemistry, in plasma by ELISA, in peripheral blood mononuclear cells by real-time PCR and flow cytometry. Effects of IL-22 on viability and gene expression of primary cultures obtained from TA…

0301 basic medicineCD4-Positive T-LymphocytesMalearterial remodelling; autoimmunity; giant cell arteritis; inflammation; interleukin-22; pathogenesismedicine.medical_treatmentMessengerInterleukin 220302 clinical medicineimmune system diseasesarterial remodelling; autoimmunity; giant cell arteritis; inflammation; interleukin-22; pathogenesis; Aged; Aged 80 and over; CD4-Positive T-Lymphocytes; Calcium Ionophores; Carcinogens; Case-Control Studies; Enzyme-Linked Immunosorbent Assay; Female; Flow Cytometry; Giant Cell Arteritis; Humans; Immunohistochemistry; In Vitro Techniques; Interleukins; Ionomycin; Leukocytes Mononuclear; Male; RNA Messenger; Real-Time Polymerase Chain Reaction; Temporal Arteries; Tetradecanoylphorbol Acetate80 and overLeukocytesPharmacology (medical)skin and connective tissue diseasesAged 80 and overIonomycinpathogenesisautoimmunityInterleukinFlow CytometryImmunohistochemistryTemporal ArteriesCalcium IonophoresCytokinecardiovascular systemTetradecanoylphorbol AcetateFemalemedicine.symptomgiant cell arteritiStromal cellMononuclearGiant Cell ArteritisInflammationEnzyme-Linked Immunosorbent AssayIn Vitro TechniquesReal-Time Polymerase Chain ReactionPeripheral blood mononuclear cellarterial remodelling03 medical and health sciencesRheumatologymedicineHumansViability assayRNA Messengercardiovascular diseasesAged030203 arthritis & rheumatologybusiness.industryInterleukinsinterleukin-22medicine.diseaseGiant cell arteritis030104 developmental biologyinflammationCase-Control StudiesImmunologyCarcinogensLeukocytes MononuclearRNAbusiness
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Sphingolipids and Inositol Phosphates Regulate the Tau Protein Phosphorylation Status in Humanized Yeast

2020

Hyperphosphorylation of protein tau is a hallmark of Alzheimer’s disease (AD). Changes in energy and lipid metabolism have been correlated with the late onset of this neurological disorder. However, it is uncertain if metabolic dysregulation is a consequence of AD or one of the initiating factors of AD pathophysiology. Also, it is unclear whether variations in lipid metabolism regulate the phosphorylation state of tau. Here, we show that in humanized yeast, tau hyperphosphorylation is stimulated by glucose starvation in coincidence with the downregulation of Pho85, the yeast ortholog of CDK5. Changes in inositol phosphate (IP) signaling, which has a central role in energy metabolism, altere…

0301 basic medicineCDK5Cèl·lulesTau proteinSit42HyperphosphorylationSaccharomyces cerevisiaeSACCHAROMYCES-CEREVISIAECeramide03 medical and health scienceschemistry.chemical_compoundCell and Developmental Biology0302 clinical medicineInositolceramideYpk1Inositol phosphatelcsh:QH301-705.51-IP7Original Researchchemistry.chemical_classificationScience & TechnologybiologyChemistryKinaseNEURODEGENERATIONLipid metabolismCell BiologyProtein phosphatase 2Fpk1MICROTUBULE-BINDINGPho85SERINE PALMITOYLTRANSFERASECell biologyALZHEIMERS-DISEASE030104 developmental biologylcsh:Biology (General)030220 oncology & carcinogenesisGLYCOGEN-SYNTHASE KINASE-3-BETAbiology.proteinKINASE-ACTIVITYPhosphorylationLife Sciences & BiomedicineBETA TOXICITYProteïnesDevelopmental BiologyFrontiers in Cell and Developmental Biology
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Aerobic Exercise and Pharmacological Treatments Counteract Cachexia by Modulating Autophagy in Colon Cancer

2016

Recent studies have correlated physical activity with a better prognosis in cachectic patients, although the underlying mechanisms are not yet understood. In order to identify the pathways involved in the physical activity-mediated rescue of skeletal muscle mass and function, we investigated the effects of voluntary exercise on cachexia in colon carcinoma (C26)-bearing mice. Voluntary exercise prevented loss of muscle mass and function, ultimately increasing survival of C26-bearing mice. We found that the autophagic flux is overloaded in skeletal muscle of both colon carcinoma murine models and patients, but not in running C26-bearing mice, thus suggesting that exercise may release the auto…

0301 basic medicineCachexiaColorectal cancerMuscle Fibers SkeletalMicevoluntary physical activityChloroquineMice Inbred BALB CMultidisciplinaryMuscle WeaknessMyogenesis3. Good healthmedicine.anatomical_structureColonic NeoplasmsFemalecancer cachexiamedicine.drugmedicine.medical_specialty[SDV.CAN]Life Sciences [q-bio]/Cancerautophagic fluxBiologyArticleCachexia03 medical and health sciencesAtrophyInternal medicineCell Line TumorPhysical Conditioning AnimalmedicineAutophagyAerobic exerciseAnimalsHumansMuscle SkeletalSirolimusrapamycinAutophagyAutophagosomesSkeletal musclemuscle wasting[SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and GastroenterologyRibonucleotidesmedicine.diseaseAminoimidazole CarboxamideSurvival Analysisexercise mimetics030104 developmental biologyEndocrinology5-amino-1-beta-D-ribofuranosyl-imidazole-4-carboxamide (AICAR)LysosomesNeoplasm Transplantationmuscle wasting; cancer cachexia; voluntary physical activity; exercise mimetics; 5-amino-1-beta-D-ribofuranosyl-imidazole-4-carboxamide (AICAR); rapamycin; autophagic flux
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Regulation of GSK-3 activity by curcumin, berberine and resveratrol: Potential effects on multiple diseases.

2017

Natural products or nutraceuticals promote anti-aging, anti-cancer and other health-enhancing effects. A key target of the effects of natural products may be the regulation of the PI3K/PTEN/Akt/mTORC1/GSK-3 pathway. This review will focus on the effects of curcumin (CUR), berberine (BBR) and resveratrol (RES), on the PI3K/PTEN/Akt/mTORC1/GSK-3 pathway, with a special focus on GSK-3. These natural products may regulate the pathway by multiple mechanisms including: reactive oxygen species (ROS), cytokine receptors, mirco-RNAs (miRs) and many others. CUR is present the root of turmeric (Curcuma longa). CUR is used in the treatment of many disorders, especially in those involving inflammatory p…

0301 basic medicineCancer ResearchCurcuminBerberinemTORC1PharmacologyResveratrolMechanistic Target of Rapamycin Complex 1Protective AgentsNatural product03 medical and health scienceschemistry.chemical_compoundGlycogen Synthase Kinase 3Phosphatidylinositol 3-KinasesBerberineGeneticNeoplasmsOsteoarthritisStilbenesGeneticsPTENHumansCurcumaMolecular BiologyProtein kinase BPI3K/AKT/mTOR pathwayInflammationNatural productsbiologyBerberine; Curcumin; Natural products; ResveratrolPTEN PhosphohydrolaseNeurodegenerative Diseasesbiology.organism_classification030104 developmental biologyBiochemistrychemistryGene Expression RegulationCardiovascular DiseasesResveratrolbiology.proteinCurcuminMolecular MedicineProto-Oncogene Proteins c-aktSignal Transduction
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Concepts to Target MYC in Pancreatic Cancer.

2016

Abstract Current data suggest that MYC is an important signaling hub and driver in pancreatic ductal adenocarcinoma (PDAC), a tumor entity with a strikingly poor prognosis. No targeted therapies with a meaningful clinical impact were successfully developed against PDAC so far. This points to the need to establish novel concepts targeting the relevant drivers of PDAC, like KRAS or MYC. Here, we discuss recent developments of direct or indirect MYC inhibitors and their potential mode of action in PDAC. Mol Cancer Ther; 15(8); 1792–8. ©2016 AACR.

0301 basic medicineCancer ResearchPoor prognosisPancreatic ductal adenocarcinomaendocrine system diseasesGene regulatory networkAntineoplastic AgentsBiologymedicine.disease_causeBioinformaticsProto-Oncogene Proteins c-myc03 medical and health sciencesPancreatic cancerCarcinomamedicineAnimalsHumansGene Regulatory NetworksMolecular Targeted TherapyProtein Kinase InhibitorsCancerGenetic Variationmedicine.diseasedigestive system diseasesGene Expression Regulation NeoplasticPancreatic Neoplasms030104 developmental biologyOncologyCarrier proteinCancer researchKRASCarrier ProteinsCarcinoma Pancreatic DuctalProtein BindingSignal TransductionMolecular cancer therapeutics
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Frequency and prognostic impact of ALK amplifications and mutations in the European Neuroblastoma Study Group (SIOPEN) high-risk neuroblastoma trial …

2021

Purpose: In neuroblastoma (NB), the ALK receptor tyrosine kinase can be constitutively activated through activating point mutations or genomic amplification. We studied ALK genetic alterations in high-risk (HR) patients on the HR-NBL1/SIOPEN trial to determine their frequency, correlation with clinical parameters, and prognostic impact. Materials and methods: Diagnostic tumor samples were available from 1,092 HR-NBL1/SIOPEN patients to determine ALK amplification status (n = 330), ALK mutational profile (n = 191), or both (n = 571). Results: Genomic ALK amplification (ALKa) was detected in 4.5% of cases (41 out of 901), all except one with MYCN amplification (MNA). ALKa was associated with …

0301 basic medicineCancer ResearchPrognostic ImpactAnaplastic Lymphoma Kinase/genetics; Child Preschool; Clinical Trials Phase III as Topic; Europe; Female; Follow-Up Studies; Gene Amplification; Humans; Infant; Male; Mutation Rate; N-Myc Proto-Oncogene Protein/genetics; Neuroblastoma/genetics; Prognosis; Randomized Controlled Trials as Topic; Risk Factors; Survival RateEuropean Neuroblastoma Study GroupSIOPENRELAPSE03 medical and health sciencesNeuroblastoma0302 clinical medicineText miningNeuroblastomahemic and lymphatic diseasesREVEALSMedicine and Health SciencesKINASEMedicineHigh risk neuroblastomaHETEROGENEITYCRIZOTINIBSEGMENTAL CHROMOSOMAL ALTERATIONSACTIVATING MUTATIONSPEDIATRIC-PATIENTSbusiness.industryALK receptor tyrosine kinasePoint mutationREARRANGEMENTSCHEMOTHERAPYmedicine.diseaseDoenças Genéticas030104 developmental biologyALKOncology030220 oncology & carcinogenesisCancer researchbusiness
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HDAC1 and HDAC2 integrate the expression of p53 mutants in pancreatic cancer.

2015

Mutation of p53 is a frequent genetic lesion in pancreatic cancer being an unmet clinical challenge. Mutants of p53 have lost the tumour-suppressive functions of wild type p53. In addition, p53 mutants exert tumour-promoting functions, qualifying them as important therapeutic targets. Here, we show that the class I histone deacetylases HDAC1 and HDAC2 contribute to maintain the expression of p53 mutants in human and genetically defined murine pancreatic cancer cells. Our data reveal that the inhibition of these HDACs with small molecule HDAC inhibitors (HDACi), as well as the specific genetic elimination of HDAC1 and HDAC2, reduce the expression of mutant p53 mRNA and protein levels. We fur…

0301 basic medicineCancer ResearchProteasome Endopeptidase ComplexMutantHistone Deacetylase 2Histone Deacetylase 1Biologymedicine.disease_causeMolecular oncologyProto-Oncogene Proteins c-myc03 medical and health sciencesMicePancreatic cancerGeneticsmedicineAnimalsHumansRNA MessengerPromoter Regions GeneticMolecular BiologyRegulation of gene expressionMice KnockoutMutationWild typeCancerProto-Oncogene Proteins c-mdm2medicine.diseaseGenes p53HDAC13. Good healthGene Expression Regulation NeoplasticHistone Deacetylase InhibitorsPancreatic NeoplasmsDisease Models Animal030104 developmental biologyMutationCancer researchOncogene
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