Search results for "colonic"

showing 10 items of 329 documents

WIN induces apoptotic cell death in human colon cancer cells through a block of autophagic flux dependent on PPARγ down-regulation.

2014

Cannabinoids have been reported to possess anti-tumorigenic activity in cancer models although their mechanism of action is not well understood. Here, we show that the synthetic cannabinoid WIN55,212-2 (WIN)-induced apoptosis in colon cancer cell lines is accompanied by endoplasmic reticulum stress induction. The formation of acidic vacuoles and the increase in LC3-II protein indicated the involvement of autophagic process which seemed to play a pro-survival role against the cytotoxic effects of the drug. However, the enhanced lysosomal membrane permeabilization (LMP) blocked the autophagic flux after the formation of autophagosomes as demonstrated by the accumulation of p62 and LC3, two ma…

Cancer ResearchMorpholinesClinical BiochemistryPharmaceutical ScienceDown-RegulationAntineoplastic AgentsApoptosisBiologyNaphthalenesDownregulation and upregulationSettore BIO/10 - BiochimicaCell Line TumormedicineAutophagyGene silencingHumansViability assayPharmacologyEndoplasmic reticulumBiochemistry (medical)AutophagyCannabinoids PPARγ ER stress autophagy/apoptosis interplay colon carcinoma cellsCell BiologyEndoplasmic Reticulum StressCell biologyBenzoxazinesMitochondriaPPAR gammaMechanism of actionApoptosisColonic NeoplasmsUnfolded protein responsemedicine.symptomSignal TransductionApoptosis : an international journal on programmed cell death
researchProduct

Redistribution of CD95, DR4 and DR5 in rafts accounts for the synergistic toxicity of resveratrol and death receptor ligands in colon carcinoma cells.

2004

The natural phytoalexin resveratrol (3, 5, 4'-trihydroxystilbene) exhibits both chemopreventive and antitumor activities through a variety of mechanisms. We have shown previously that resveratrol-induced apoptosis of a human colon cancer cell line involved the redistribution of CD95 (Fas/Apo-1) into lipid rafts. Here, we show that, in colon cancer cells that resist to resveratrol-induced apoptosis, the polyphenol also induces a redistribution of death receptors into lipid rafts. This effect sensitizes these tumor cells to death receptor-mediated apoptosis. In resveratrol-treated cells, tumor necrosis factor (TNF), anti-CD95 antibodies and TNF-related apoptosis-inducing ligand (TRAIL) activa…

Cancer ResearchNystatinTime FactorsApoptosisResveratrolmedicine.disease_causeLigandsReceptors Tumor Necrosis FactorTNF-Related Apoptosis-Inducing Ligandchemistry.chemical_compoundStilbenesReceptorLipid raftCaspaseMembrane GlycoproteinsbiologyFas receptorFlow CytometryLipidsMitochondriaProto-Oncogene Proteins c-bcl-2CaspasesColonic Neoplasmslipids (amino acids peptides and proteins)Tumor necrosis factor alphaSignal Transductionmedicine.medical_specialtyBlotting WesternTransfectionMembrane MicrodomainsInternal medicineCell Line TumorGeneticsmedicineHumansfas ReceptorMolecular BiologyTumor Necrosis Factor-alphaCarcinomaLipid MetabolismAntineoplastic Agents PhytogenicReceptors TNF-Related Apoptosis-Inducing LigandEndocrinologychemistryApoptosisResveratrolCancer researchbiology.proteinCarcinogenesisApoptosis Regulatory ProteinsOncogene
researchProduct

Mast Cells Infiltrating Inflamed or Transformed Gut Alternatively Sustain Mucosal Healing or Tumor Growth.

2015

Abstract Mast cells (MC) are immune cells located next to the intestinal epithelium with regulatory function in maintaining the homeostasis of the mucosal barrier. We have investigated MC activities in colon inflammation and cancer in mice either wild-type (WT) or MC-deficient (KitW-sh) reconstituted or not with bone marrow-derived MCs. Colitis was chemically induced with dextran sodium sulfate (DSS). Tumors were induced by administering azoxymethane (AOM) intraperitoneally before DSS. Following DSS withdrawal, KitW-sh mice showed reduced weight gain and impaired tissue repair compared with their WT littermates or KitW-sh mice reconstituted with bone marrow-derived MCs. MCs were localized i…

Cancer ResearchPathologyColorectal cancerCell CountAnimals; Animals Congenic; Azoxymethane; Carcinoma; Cell Count; Cell Transformation Neoplastic; Cells Cultured; Colitis; Colonic Neoplasms; Dextran Sulfate; Epithelial Cells; Humans; Inflammatory Bowel Diseases; Interleukin-33; Intestinal Mucosa; Mast Cells; Mice; Mice Inbred C57BL; Mice Knockout; Models Biological; Proto-Oncogene Proteins c-kit; Receptors Interleukin; Regeneration; Serine Endopeptidases; Species Specificity; Specific Pathogen-Free Organisms; Cancer Research; Oncology; Medicine (all)chemistry.chemical_compoundMiceAnimals CongenicMast CellMast CellsIntestinal MucosaCells CulturedMice KnockoutColonic NeoplasmMedicine (all)Dextran SulfateSerine EndopeptidasesColitisIntestinal epitheliumSpecific Pathogen-Free OrganismsSerine EndopeptidaseProto-Oncogene Proteins c-kitCell Transformation NeoplasticOncologyColonic Neoplasmsmedicine.symptomHumanmedicine.medical_specialtyAzoxymethaneInflammationModels BiologicalImmune systemSpecies SpecificitymedicineSpecific Pathogen-Free OrganismAnimalsHumansRegenerationColitisEpithelial CellAnimalAzoxymethanebusiness.industryInflammatory Bowel DiseaseCarcinomaEpithelial CellsReceptors Interleukinmedicine.diseaseInflammatory Bowel DiseasesInterleukin-33Interleukin-1 Receptor-Like 1 ProteinMice Inbred C57BLchemistrybusinessWound healingColitiHomeostasisCancer research
researchProduct

Mechanisms of tumor invasion: evidence from in vivo observations.

1985

The major mechanisms of tumor invasion in vivo are discussed in the present review. A special emphasis is placed on tumor dedifferentiation which has proved to be of paramount importance for the invasion process. Based on in vivo observations obtained from various human and animal tumors a concept for the mechanism of tumor invasion is proposed which mainly comprises the following basic events: the first and essential step in tumor invasion is the tumor dedifferentiation and dissociation at the invasion front. This apparently temporary and reversible process mobilizes the tumor cells out of the main tumor bulk and enables them to invade the host tissue by active locomotion. This mechanism i…

Cancer ResearchPathologymedicine.medical_specialtyCell divisionColonCellular differentiationBiologyHost tissueBasement MembraneExtracellular matrixIn vivoCell MovementmedicineAnimalsEdemaHumansNeoplasm InvasivenessProcess (anatomy)Cells CulturedDimethylhydrazinesCell DifferentiationMuscle SmoothCell biology12-DimethylhydrazineExtracellular MatrixNeoplasm ProteinsRatsOxygenInterstitial edemaIntercellular JunctionsOncologyColonic NeoplasmsAtrophyIntracellularCell DivisionPeptide HydrolasesCancer metastasis reviews
researchProduct

Metabolic Imaging in Microregions of Tumors and Normal Tissues With Bioluminescence and Photon Counting

1988

A method has been developed for metabolic imaging on a microscopic level in tumors, tumor spheroids, and normal tissues. The technique makes it possible to determine the spatial distribution of glucose, lactate, and ATP in absolute terms at similar locations within tissues or cell aggregates. The substrate distributions are registered in serial cryostat sections from tissue cryobiopsies or from frozen spheroids with the use of bioluminescence reactions. The light emission is measured directly by a special imaging photon counting system enabling on-line image analysis. The technique has been applied to human breast cancer xenografts, to spheroids originating from a human colon adenocarcinoma…

Cancer ResearchPathologymedicine.medical_specialtyCellBiologyAdenosine TriphosphateNeoplasmsmedicineMedical imagingAnimalsHumansBioluminescenceLarge intestineLactic AcidRadionuclide ImagingRadiationMusclesSpheroidMammary Neoplasms Experimentalmedicine.diseasePhoton countingRatsGlucosemedicine.anatomical_structureOncologyColonic NeoplasmsLuminescent MeasurementsLactatesBiophysicsAdenocarcinomaFemaleLight emissionJNCI Journal of the National Cancer Institute
researchProduct

Comparative study of human colonic tumor-derived endothelial cells (HCTEC) and normal colonic microvascular endothelial cells (HCMEC): Hypoxia-induce…

2009

Colorectal carcinoma growth and progression is dependent on the vasculature of the tumor microenvironment. Tumor-derived endothelial cells differ functionally from their normal counterpart. For this reason we isolated microvascular endothelial cells from human colon cancer tissue (HCTEC) and compared them with endothelial cells from normal colonic tissue (HCMEC) of the same donor. Since hypoxia is a universal hallmark of carcinomas, we examined its effects on HCTEC of five patients in comparison with the corresponding HCMEC, with respect to the secretion of the soluble form of the two important vascular endothelial growth factor (VEGF) receptors, VEGFR-1 and -2. After dissociation by dispas…

Cancer ResearchPathologymedicine.medical_specialtyEndotheliumColonEnzyme-Linked Immunosorbent AssayCell SeparationBiologychemistry.chemical_compoundmedicineHumansCells CulturedTumor microenvironmentVascular Endothelial Growth Factor Receptor-1OncogeneMicrocirculationEndothelial CellsGeneral MedicineVascular Endothelial Growth Factor Receptor-2Cell HypoxiaEndothelial stem cellVascular endothelial growth factormedicine.anatomical_structureOncologychemistryApoptosisTumor progressionColonic NeoplasmsCancer researchTumor necrosis factor alphaOncology Reports
researchProduct

Aurora-A Transcriptional Silencing and Vincristine Treatment Show a Synergistic Effect in Human Tumor Cells

2008

Aurora-A is a centrosome-associated serine/threonine kinase that is overexpressed in multiple types of human tumors. Primarily, Aurora-A functions in centrosome maturation and mitotic spindle assembly. Overexpression of Aurora-A induces centrosome amplification and G 2 /M cell cycle progression. Recently, it was observed that overexpression of Aurora-A renders cells resistant to cisplatin (CDDP)-, etoposide-, and paclitaxel-induced apoptosis.Our results indicate that already in initial stages of cancer progression Aurora-A overexpression could have a major role in inducing supernumerary centrosomes and aneuploidy, as shown by immunohistochemistry on tissue sections from various stages of hu…

Cancer ResearchPathologymedicine.medical_specialtyTranscription GeneticApoptosismacromolecular substancesProtein Serine-Threonine KinasesBiologyTransfectionPLK1Aurora KinasesRNA interferenceCell Line TumormedicineHumansGene silencingGene SilencingRNA Small InterferingMitotic catastropheCentrosomeCisplatinCarcinomaCell CycleDrug SynergismAuroraA/stk15centrosome amplificationAneuploidy CINGeneral MedicineCell cycleAneuploidyAntineoplastic Agents PhytogenicGene Expression Regulation NeoplasticSettore BIO/18 - Geneticaenzymes and coenzymes (carbohydrates)OncologyVincristineCentrosomeColonic Neoplasmsembryonic structuresCancer cellCancer researchbiological phenomena cell phenomena and immunityHeLa Cellsmedicine.drugOncology Research Featuring Preclinical and Clinical Cancer Therapeutics
researchProduct

Intestinal epithelial HuR modulates distinct pathways of proliferation and apoptosis and attenuates small intestinal and colonic tumor development.

2014

Abstract HuR is a ubiquitous nucleocytoplasmic RNA-binding protein that exerts pleiotropic effects on cell growth and tumorigenesis. In this study, we explored the impact of conditional, tissue-specific genetic deletion of HuR on intestinal growth and tumorigenesis in mice. Mice lacking intestinal expression of HuR (Hur IKO mice) displayed reduced levels of cell proliferation in the small intestine and increased sensitivity to doxorubicin-induced acute intestinal injury, as evidenced by decreased villus height and a compensatory shift in proliferating cells. In the context of Apcmin/+ mice, a transgenic model of intestinal tumorigenesis, intestinal deletion of the HuR gene caused a three-fo…

Cancer ResearchPost-translational regulationRNA-binding proteinContext (language use)ApoptosisCell Growth ProcessesBiologymedicine.disease_causeArticleAU-rich RNAMiceGene expressionIntestinal NeoplasmsmedicineAnimalsmRNA stabilityIntestinal MucosaMice KnockoutCell growthMolecular biologyPhenotypeProtein-RNA interactionSmall intestineDisease Models Animalmedicine.anatomical_structureOncologyELAV ProteinsApoptosisColonic NeoplasmsCancer researchCarcinogenesis
researchProduct

The role of oxidative stress in apoptosis induced by the histone deacetylase inhibitor suberoylanilide hydroxamic acid in human colon adenocarcinoma …

2008

Histone deacetylase inhibitors (HDACIs) activate genes that promote cell cycle arrest and apoptosis in a number of tumor cells. This study showed that suberoylanilide hydroxamic acid (SAHA), a potent and commonly used HDACI, induced apoptosis in human colon adenocarcinoma HT-29 cells in a time- and dose-dependent manner. This effect was accompanied by the induction of oxidative stress, dissipation of mitochondrial transmembrane potential and activation of executioner caspases. Moreover, SAHA increased the levels of phosphorylated active forms of p38 and JNK. The addition of either the antioxidant N-acetylcysteine or the specific inhibitor of NADPH oxidase diphenylene iodonium chloride reduc…

Cancer ResearchProgrammed cell deathmedicine.drug_classCell Survivalp38 mitogen-activated protein kinasesBlotting WesternApoptosisAdenocarcinomamedicine.disease_causeHydroxamic AcidsAntioxidantsSettore BIO/10 - BiochimicamedicineHumansEnzyme InhibitorsProtein kinase BCaspaseMembrane Potential MitochondrialVorinostatbiologyHistone deacetylase inhibitorEnzyme ActivationHistone Deacetylase InhibitorsOxidative StressOncologyBiochemistryApoptosisCaspasesColonic NeoplasmsCancer researchbiology.proteinHistone deacetylaseReactive Oxygen Speciescolon adenomacarcinoma cells histone deacetylase inhibitors apoptosisHT29 CellsOxidative stressSignal TransductionInternational journal of oncology
researchProduct

EURECCA colorectal: multidisciplinary management: European consensus conference colon & rectum.

2014

Contains fulltext : 137861.pdf (Publisher’s version ) (Closed access) BACKGROUND: Care for patients with colon and rectal cancer has improved in the last 20years; however considerable variation still exists in cancer management and outcome between European countries. Large variation is also apparent between national guidelines and patterns of cancer care in Europe. Therefore, EURECCA, which is the acronym of European Registration of Cancer Care, is aiming at defining core treatment strategies and developing a European audit structure in order to improve the quality of care for all patients with colon and rectal cancer. In December 2012, the first multidisciplinary consensus conference about…

Cancer ResearchQuality Assurance Health CareColorectal cancerCancer development and immune defence Radboud Institute for Molecular Life Sciences [Radboudumc 2]Delphi methodSurgical oncologyFAMILIAL ADENOMATOUS POLYPOSISTumours of the digestive tract Radboud Institute for Molecular Life Sciences [Radboudumc 14]MedicineSHORT-COURSE RADIOTHERAPYRectal cancerQuality assurance; Colon cancer; Rectal cancer; Multidisciplinary teams; Consensus; Delphi method; Audit; Neoadjuvant treatment; Adjuvant treatment; SurgerySettore MED/36 - DIAGNOSTICA PER IMMAGINI E RADIOTERAPIADisease ManagementPHASE-III TRIALRANDOMIZED CONTROLLED-TRIALNeoadjuvant TherapyQuality assuranceColon cancerEuropemedicine.anatomical_structureTreatment OutcomeOncologyTRANSANAL ENDOSCOPIC MICROSURGERYColonic NeoplasmsPractice Guidelines as TopicHYPERTHERMIC INTRAPERITONEAL CHEMOTHERAPYmedicine.medical_specialtyNeoadjuvant treatmentEvidence-based practiceConsensusLYMPH-NODE EVALUATIONDelphi methodRectumAuditSDG 3 - Good Health and Well-beingHumansCIRCUMFERENTIAL RESECTION MARGINddc:610business.industryRectal NeoplasmsTOTAL MESORECTAL EXCISIONCancerLONG-TERM SURVIVALAuditAdjuvant treatmentmedicine.diseaseSurgeryOncology nursingFamily medicineSurgeryMultidisciplinary teamsbusiness
researchProduct