Search results for "tumori"

showing 10 items of 62 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
researchProduct

MYC-driven epigenetic reprogramming favors the onset of tumorigenesis by inducing a stem cell-like state

2018

Breast cancer consists of highly heterogeneous tumors, whose cell of origin and driver oncogenes are difficult to be uniquely defined. Here we report that MYC acts as tumor reprogramming factor in mammary epithelial cells by inducing an alternative epigenetic program, which triggers loss of cell identity and activation of oncogenic pathways. Overexpression of MYC induces transcriptional repression of lineage-specifying transcription factors, causing decommissioning of luminal-specific enhancers. MYC-driven dedifferentiation supports the onset of a stem cell-like state by inducing the activation of de novo enhancers, which drive the transcriptional activation of oncogenic pathways. Furthermo…

0301 basic medicineCarcinogenesisScienceGeneral Physics and AstronomyBreast NeoplasmsMice SCIDTumor initiationBiologyBreast cancer MYC Tumorigenesismedicine.disease_causeArticleGeneral Biochemistry Genetics and Molecular BiologyEpigenesis GeneticProto-Oncogene Proteins c-mycMice03 medical and health sciencesCell Line TumormedicineAnimalsHumansEpigeneticslcsh:ScienceEnhancerTranscription factorRegulation of gene expressionMultidisciplinaryQGeneral ChemistryCellular ReprogrammingCell biologyGene Expression Regulation NeoplasticEnhancer Elements Genetic030104 developmental biologyNeoplastic Stem CellsFemalelcsh:QStem cellCarcinogenesisReprogramming
researchProduct

[How some commensal bacteria would exacerbate colorectal carcinogenesis?].

2016

International audience; The gut microbiota maintains a relationship with its host with strong mutual benefits. Changes in the composition of the intestinal microbiota have been detected in colorectal cancer patients to the extent that it is now considered as a real contributing factor in this pathology. In this review, we focus on three commensal bacterial species, namely Bacteroides fragilis, Fusobacterium nucleatum, and Escherichia coli, which seem to emerge as pathogens and to contribute to colorectal carcinogenesis through their inflammatory and oncogenic properties.; Le microbiote intestinal entretient une relation mutualiste forte avec l’hôte. Depuis la mise en évidence de modificatio…

0301 basic medicineColorectal cancer[SDV]Life Sciences [q-bio]enterotoxigenic bacteroides-fragilis[SDV.CAN]Life Sciences [q-bio]/Cancer[ SDV.MP.BAC ] Life Sciences [q-bio]/Microbiology and Parasitology/BacteriologyGut floradnamedicine.disease_causeGeneral Biochemistry Genetics and Molecular Biology[ SDV.CAN ] Life Sciences [q-bio]/CancerMicrobiology03 medical and health sciences0302 clinical medicine[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologymedicineEscherichia colimucosatumorisgenesisComputingMilieux_MISCELLANEOUSGastrointestinal tract[ SDV ] Life Sciences [q-bio]biologyfusobacterium-nucleatumHost (biology)General Medicinebiology.organism_classificationmedicine.disease[SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriologymicroenvironment3. Good healthstomatognathic diseasestumorigenesis030104 developmental biologyinflammation030220 oncology & carcinogenesisgutcellsBacteroides fragilisFusobacterium nucleatumCarcinogenesiscolon-cancer[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
researchProduct

Silencing of hepatic fate-conversion factors induce tumorigenesis in reprogrammed hepatic progenitor-like cells

2016

Abstract Background Several studies have reported the direct conversion of mouse fibroblasts to hepatocyte-like cells with different degrees of maturation by expression of hepatic fate-conversion factors. Methods We have used a combination of lentiviral vectors expressing hepatic fate-conversion factors with Oct4, Sox2, Klf4, and Myc to convert mouse embryonic fibroblasts into hepatic cells. Results We have generated hepatic cells with progenitor-like features (iHepL cells). iHepL cells displayed basic hepatocyte functions but failed to perform functions characteristic of mature hepatocytes such as significant Cyp450 or urea cycle activities. iHepL cells expressed multiple hepatic-specific …

0301 basic medicineMaleCarcinogenesisCellular differentiationMedicine (miscellaneous)Gene ExpressionReceptors G-Protein-CoupledMiceMice Inbred NODHepatocyteTransgenesStem CellsTeratomaCell DifferentiationForkhead Transcription FactorsCellular ReprogrammingCell biologyKLF4Molecular MedicineStem cellReprogrammingDirect reprogrammingGenetic VectorsKruppel-Like Transcription FactorsBiologyBiochemistry Genetics and Molecular Biology (miscellaneous)Proto-Oncogene Proteins c-myc03 medical and health sciencesKruppel-Like Factor 4SOX2AnimalsHepatectomyGene SilencingProgenitor cellResearchXenograftSOXB1 Transcription FactorsLentivirusCD24 AntigenCell BiologyFibroblastsEmbryo MammalianEmbryonic stem cell030104 developmental biologyTumorigenesisHepatic stellate cellHepatocytesOctamer Transcription Factor-3BiomarkersProgenitorStem Cell Research & Therapy
researchProduct

DNA methylation changes and somatic mutations as tumorigenic events in Lynch syndrome-associated adenomas retaining mismatch repair protein expression

2018

Background: DNA mismatch repair (MMR) defects are a major factor in colorectal tumorigenesis in Lynch syndrome (LS) and 15% of sporadic cases. Some adenomas from carriers of inherited MMR gene mutations have intact MMR protein expression implying other mechanisms accelerating tumorigenesis. We determined roles of DNA methylation changes and somatic mutations in cancer-associated genes as tumorigenic events in LS-associated colorectal adenomas with intact MMR. Methods: We investigated 122 archival colorectal specimens of normal mucosae, adenomas and carcinomas from 57 LS patients. MMR-deficient (MMR-D, n 49) and MMR-proficient (MMR-P, n 18) adenomas were of particular interest and were inter…

0301 basic medicineMaleResearch paperMICROSATELLITE INSTABILITYHYPOMETHYLATIONDNA mismatch repairPHENOTYPEmedicine.disease_causeEpigenesis Genetic0302 clinical medicineCOLORECTAL ADENOMASCDKN2APromoter Regions Geneticcolorectal adenomaDNA methylationLINE-1 methylationTumor suppressorGeneral MedicineMethylationMiddle AgedCANCERTUMORSLynch syndromeDNA-metylaatio3. Good healthDEFICIENCY030220 oncology & carcinogenesisDNA methylationsyöpätauditFemaleColorectal adenomaAdultcongenital hereditary and neonatal diseases and abnormalitiesAdenomatumor suppressorsuolistosyövätColorectal adenomaBiologycomplex mixturesGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesBRAF MUTATIONmedicineHumansLynchin oireyhtymäAgedTumor Suppressor ProteinsMicrosatellite instabilityDNAUNE-1 methylationta3122medicine.diseaseGENEColorectal Neoplasms Hereditary Nonpolyposisdigestive system diseasestumorigenesisCOPY NUMBER030104 developmental biologyLynch syndromeLong Interspersed Nucleotide Elements3121 General medicine internal medicine and other clinical medicineMutationTumorigenesisCancer research3111 BiomedicineTumotigenesismutationCarcinogenesisEBioMedicine
researchProduct

Molecular chaperones in tumors of salivary glands.

2020

The salivary glands are key components of the mouth and play a central role in its physiology. Their importance may be appreciated considering their number, occurrence in pairs, and distribution in the mouth: two parotids, two submandibular, two sublingual, and many other small ones scattered throughout the mouth. They produce saliva, without which ingestion of non-liquid nutrients and speech would be practically impossible. Nevertheless, the physiology and pathology of salivary glands are poorly understood. For instance, tumors of salivary glands occur, and their incidence is on the rise, but their etiology and pathogenesis are virtually unknown, although some risk factors have been identi…

0301 basic medicineSalivaHistologyPhysiologyDifferential diagnosiBiologyBioinformaticsmedicine.disease_causePathogenesis03 medical and health sciencesstomatognathic systemmedicineHSPAnimalsHumansEndoplasmic Reticulum Chaperone BiPTumorsSalivary glandTumorigenesiChaperoning system030102 biochemistry & molecular biologySalivary glandCell BiologyGeneral MedicineSalivary Gland Neoplasms030104 developmental biologymedicine.anatomical_structureCell Transformation NeoplasticChaperone (protein)Etiologybiology.proteinMolecular chaperoneBiomarker (medicine)Disease SusceptibilityDifferential diagnosisCarcinogenesisMolecular ChaperonesJournal of molecular histology
researchProduct

Non-coding RNAs Functioning in Colorectal Cancer Stem Cells

2016

In recent years, the hypothesis of the presence of tumor-initiating cancer stem cells (CSCs) has received a considerable support. This model suggested the existence of CSCs which, thanks to their self-renewal properties, are able to drive the expansion and the maintenance of malignant cell populations with invasive and metastatic potential in cancer. Increasing evidence showed the ability of such cells to acquire self-renewal, multipotency, angiogenic potential, immune evasion, symmetrical and asymmetrical divisions which, along with the presence of several DNA repair mechanisms, further enhance their oncogenic potential making them highly resistant to common anticancer treatments. The main…

0301 basic medicinemedicine.disease_cause03 medical and health sciences0302 clinical medicineCancer stem cellEpithelialmesenchymal transitionmicroRNAmedicineEpithelial–mesenchymal transitionSonic hedgehogNon-coding RNACancer stem cells; Colorectal cancer; Differentiation; Epithelialmesenchymal transition; MicroRNAs; Non-coding RNAs; Self-renewal; Signaling pathways; Stemness; Tumorigenicity; Medicine (all); Biochemistry Genetics and Molecular Biology (all)TumorigenicityStemneBiochemistry Genetics and Molecular Biology (all)biologySignaling pathwayCancer stem cellMedicine (all)Wnt signaling pathwayCancerMicroRNAmedicine.diseaseColorectal cancerCell biology030104 developmental biologyDifferentiation030220 oncology & carcinogenesisbiology.proteinSelf-renewalStem cellCarcinogenesis
researchProduct

Deciphering genomic heterogeneity and the internal composition of tumour activities through a hierarchical factorisation model

2021

Genomic heterogeneity constitutes one of the most distinctive features of cancer diseases, limiting the efficacy and availability of medical treatments. Tumorigenesis emerges as a strongly stochastic process, producing a variable landscape of genomic configurations. In this context, matrix factorisation techniques represent a suitable approach for modelling such complex patterns of variability. In this work, we present a hierarchical factorisation model conceived from a systems biology point of view. The model integrates the topology of molecular pathways, allowing to simultaneously factorise genes and pathways activity matrices. The protocol was evaluated by using simulations, showing a hi…

:Informàtica::Aplicacions de la informàtica::Bioinformàtica [Àrees temàtiques de la UPC]Matrix factorisationComputer scienceBioinformaticsGeneral MathematicsSystems biologyPopulationMatrix factorisationContext (language use)Computational biologyComputational biologyGenomic heterogeneitygenomic heterogeneityFactorizationBioinformàticaSimulació per ordinadorComputer Science (miscellaneous)QA1-939cancerVariabilityeducationEngineering (miscellaneous)Topology (chemistry)Cancereducation.field_of_studyvariabilitymatrix factorisationLimitingbioinformaticsCàncer--Aspectes genèticsGenòmicaBreast--CancerTumorigenesisMathematics
researchProduct

Alimentazione e tumori

2008

Alimentazione tumori alimentiSettore BIO/09 - Fisiologia
researchProduct

Imaging con trattografia nella pianificazione chirurgica delle neoplasie cerebrali: esperienza preliminare.

2007

Poster congresso nazionale AINR. Bergamo, 20-23 Giugno 2007

DTI trattografia tumori encefaliciSettore MED/36 - Diagnostica Per Immagini E Radioterapia
researchProduct