Search results for "colonic"

showing 10 items of 329 documents

Follow-up of patients with colonic polyps containing severe atypia and invasive carcinoma. Compliance, recurrence, and survival

1988

Between January 1975 and December 1984 1769 polyps were endoscopically removed from 1219 patients. Eight percent of these patients had polyps containing severe atypia and 5.0% had polyps containing invasive cancer. A close postoperative surveillance program was followed by only a few patients, but compliance improved with longer follow-up intervals. Metachronous polyps were observed with similar frequency in patients with benign polyps (34.8%) and those with polyps containing severe atypia (23.8%) or cancer (41.7%). Patients in whom malignant polyps were endoscopically removed had a 5-year survival rate of 84.3% that did not differ from that of patients' whose polyps contained severe atypia…

Cancer Researchmedicine.medical_specialtyColonic PolypsGastroenterologyActuarial AnalysisInternal medicineotorhinolaryngologic diseasesmedicineAtypiaCarcinomaHumansNeoplasm InvasivenessPatient complianceneoplasmsSurvival rateAgedRetrospective StudiesInvasive carcinomaEpitheliomabusiness.industryCarcinomaCancerEndoscopypathological conditions signs and symptomsMiddle Agedmedicine.diseasedigestive system diseasesBenign polypsSurgerysurgical procedures operativeOncologyPopulation SurveillancePatient ComplianceNeoplasm Recurrence LocalbusinessFollow-Up StudiesCancer
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Resistance factors in colon cancer tissue and the adjacent normal colon tissue: glutathione S-transferases alpha and pi, glutathione and aldehyde deh…

1998

Abstract Glutathione S -transferases (GST) α and π , glutathione (GSH) and aldehyde dehydrogenase (ADH) were determined in colorectal cancer tissue specimens and in the adjacent normal colon tissue. The median contents in normal and cancer tissue were 8.1 (2.3–30.3) (5–95% quantiles) and 15.1 (5.3–50.3) μ g/mg protein for GST π ( P =0.035), 0.0 (0.0–1.4) and 0.4 (0.0–3.5) μ g/mg protein for GST α ( P =0.019), 7.3 (1.3–22.7) and 5.6 (2.3–26.0) μ g/mg protein for GSH ( P =0.171) and 30.8 (13.0–42.0) and 23.2 (9.0–32.9) μ g/mg protein for ADH ( P =0.0017), respectively. Thus, the mean GST α and π both significantly increased in colon cancer compared to the adjacent normal tissue, which underli…

Cancer Researchmedicine.medical_specialtyColorectal cancerColonAldehyde dehydrogenaseBiologymedicine.disease_causeIsozymeGene productchemistry.chemical_compoundInternal medicineGene expressionmedicineHumansGlutathione TransferaseCancerGlutathioneAldehyde Dehydrogenasemedicine.diseaseGlutathioneEndocrinologyOncologychemistryDrug Resistance NeoplasmColonic Neoplasmsbiology.proteinCarcinogenesisCancer letters
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Mast cells boost myeloid-derived suppressor cell activity and contribute to the development of tumor-favoring microenvironment

2014

Abstract Inflammation plays crucial roles at different stages of tumor development and may lead to the failure of immune surveillance and immunotherapy. Myeloid-derived suppressor cells (MDSC) are one of the major components of the immune-suppressive network that favors tumor growth, and their interaction with mast cells is emerging as critical for the outcome of the tumor-associated immune response. Herein, we showed the occurrence of cell-to-cell interactions between MDSCs and mast cells in the mucosa of patients with colon carcinoma and in the colon and spleen of tumor-bearing mice. Furthermore, we demonstrated that the CT-26 colon cancer cells induced the accumulation of CD11b+Gr1+ imma…

Cancer Researchmedicine.medical_treatmentCD40 LigandImmunologyInflammationCell CommunicationBiologyNitric OxideProinflammatory cytokineInterferon-gammaMiceImmune systemAntigens CD40Animals; Antigens CD40; CD40 Ligand; Cell Line Tumor; Colonic Neoplasms; Humans; Inflammation; Interferon-gamma; Mast Cells; Mice; Mice Inbred BALB C; Mice Knockout; Myeloid Cells; Nitric Oxide; Tumor Microenvironment; Cell Communication; Cancer Research; Immunology; Medicine (all)Cell Line TumormedicineMast cell; Myeloid-Derived Suppressor Cell; tumor microenvironment; colon cancerTumor MicroenvironmentAnimalsHumansMyeloid-Derived Suppressor CellMast CellMyeloid CellsMast CellsCD40 AntigensMyeloid CellInflammationMice KnockoutTumor microenvironmentColonic NeoplasmMice Inbred BALB CCD40AnimalMedicine (all)ImmunotherapyMast cellmedicine.anatomical_structurecolon cancerImmunologyColonic NeoplasmsCancer researchMyeloid-derived Suppressor Cellbiology.proteinmedicine.symptomHuman
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Flt3 ligand lessens the growth of tumors obtained after colon cancer cell injection in rats but does not restore tumor-suppressed dendritic cell func…

2000

A defective function of the antigen-presenting cells may represent one of the ways used by cancer cells to escape the immune response. We have previously shown that human and rat colon carcinomas were infiltrated by dendritic cells that did not express the B7 co-stimulatory molecules required for inducing an efficient T-cell response. Flt3 ligand is a cloned hematopoietic growth factor that markedly augments the number of functional dendritic and NK cells in lymphoid and non-lymphoid tissues and exerts anti-tumor activity in various experimental models. We show here that repeated Flt3 ligand administration delays the s.c. growth of rat colon cancer cells in syngeneic animals without inducin…

Cancer Researchmedicine.medical_treatmentHematopoietic growth factorAntineoplastic AgentsBiologyLymphocyte ActivationNatural killer cellMiceImmune systemmedicineAnimalsAntigen PresentationFollicular dendritic cellsGrowth factorMembrane ProteinsDendritic CellsDendritic cellRatsKiller Cells Naturalmedicine.anatomical_structureOncologyColonic NeoplasmsCancer cellImmunologyInterleukin 12Cancer researchNeoplasm TransplantationSpleenInternational Journal of Cancer
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Experimental evolution of an oncolytic vesicular stomatitis virus with increased selectivity for p53-deficient cells

2014

Experimental evolution has been used for various biotechnological applications including protein and microbial cell engineering, but less commonly in the field of oncolytic virotherapy. Here, we sought to adapt a rapidly evolving RNA virus to cells deficient for the tumor suppressor gene p53, a hallmark of cancer cells. To achieve this goal, we established four independent evolution lines of the vesicular stomatitis virus (VSV) in p53-knockout mouse embryonic fibroblasts (p53-/- MEFs) under conditions favoring the action of natural selection. We found that some evolved viruses showed increased fitness and cytotoxicity in p53-/- cells but not in isogenic p53+/+ cells, indicating gene-specifi…

Cancer TreatmentVirus OncolíticosProtein EngineeringMiceMedicine and Health SciencesMacromolecular EngineeringMice KnockoutOncolytic VirotherapyMultidisciplinaryQProteína p53 Supresora de TumorRNeoplasias de la Mama3. Good healthOncolytic VirusesOncologyVesicular stomatitis virusColonic NeoplasmsMedicineFemaleVesicular StomatitisResearch ArticleBiotechnologyDirected EvolutionEvolutionary ProcessesTumor suppressor geneScienceBioengineeringBreast NeoplasmsBiologyMicrobiologyViral EvolutionVirusVesicular StomatitisVirologyCell Line TumorGeneticsAnimalsHumansEvolutionary BiologyNeoplasias del ColonBiology and Life SciencesRNA virusVesiculovirusbiology.organism_classificationVirologyOrganismal EvolutionOncolytic virusAnimal Models of InfectionArtificial SelectionSynthetic BioengineeringViruses and CancerCell cultureMicrobial EvolutionCancer cellCancer researchDirected Molecular EvolutionTumor Suppressor Protein p53
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Increased endocannabinoid levels reduce the development of precancerous lesions in the mouse colon

2007

Colorectal cancer is an increasingly important cause of death in Western countries. Endocannabinoids inhibit colorectal carcinoma cell proliferation in vitro. In this paper, we investigated the involvement of endocannabinoids on the formation of aberrant crypt foci (ACF, earliest preneoplastic lesions) in the colon mouse in vivo. ACF were induced by azoxymethane (AOM); fatty acid amide hydrolase (FAAH) and cannabinoid receptor messenger ribonucleic acid (mRNA) levels were analyzed by the quantitative reverse transcription polymerase chain reaction (RT-PCR); endocannabinoid levels were measured by liquid chromatography-mass spectrometry; caspase-3 and caspase-9 expressions were measured by W…

Cannabinoid receptormedicine.medical_treatment2-Arachidonoylglycerolpreneoplastic lesionsMass Spectrometrychemistry.chemical_compoundMice0302 clinical medicineFatty acid amide hydrolaseDrug DiscoveryFatty acid amide hydrolase (FAAH)Aberrant crypt fociGenetics(clinical)ReceptorReceptors CannabinoidGenetics (clinical)Medicine(all)0303 health sciencesCaspase 3Reverse Transcriptase Polymerase Chain ReactionEndocannabinoid systemCaspase 93. Good health2-arachidonoylglycerolColon cancer030220 oncology & carcinogenesisColonic NeoplasmsMolecular Medicinelipids (amino acids peptides and proteins)psychological phenomena and processesRapid CommunicationAberrant crypt focimedicine.medical_specialtyColonAzoxymethaneBiologydigestive systemAmidohydrolases03 medical and health sciencesInternal medicineCannabinoid Receptor ModulatorsmedicineAnimalsRNA MessengerCannabinoid receptors030304 developmental biologyAzoxymethaneendocannabinoiddigestive system diseasesEndocrinologychemistrynervous systemCancer researchCannabinoidcancer pharmacologyPrecancerous ConditionsEndocannabinoids
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Development and application of test methods for the detection of dietary constituents which protect against heterocyclic aromatic amines

2003

This article describes the development and use of assay models in vitro (genotoxicity assay with genetically engineered cells and human hepatoma (HepG2) cells) and in vivo (genotoxicity and short-term carcinogenicity assays with rodents) for the identification of dietary constituents which protect against the genotoxic and carcinogenic effects of heterocyclic aromatic amines (HAs). The use of genetically engineered cells expressing enzymes responsible for the bioactivation of HAs enables the detection of dietary factors that inhibit the metabolic activation of HAs. Human derived hepatoma (HepG2) cells are sensitive towards HAs and express several enzymes [glutathione S-transferase (GST), N-…

Carcinoma HepatocellularDNA damage[SDV]Life Sciences [q-bio]Health Toxicology and Mutagenesismedicine.disease_causeIsozyme03 medical and health sciences0302 clinical medicineANTICARCINOGENEHeterocyclic CompoundsIn vivoTumor Cells CulturedGeneticsmedicineAnticarcinogenic AgentsHumansMolecular BiologyAnticarcinogenComputingMilieux_MISCELLANEOUSCarcinogen030304 developmental biologychemistry.chemical_classification0303 health sciencesChemistryLiver NeoplasmsCANCERIn vitroDietEFFET PROTECTEUREnzymeBiochemistry030220 oncology & carcinogenesisColonic NeoplasmsFood AnalysisGenotoxicityMutation Research/Fundamental and Molecular Mechanisms of Mutagenesis
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Inhibitory effects oftrans-resveratrol analogs molecules on the proliferation and the cell cycle progression of human colon tumoral cells

2008

International audience; Resveratrol may function as a cancer chemopreventive agent. However, few data are available on the antitumoral activities of its dimer, epsilon-viniferin, also present in human diet. So, the effects of resveratrol, epsilon-viniferin, of their acetylated forms (resveratrol triacetate, epsilon-viniferin pentaacetate) and of vineatrol (a wine grape extract) were compared on human adenocarcinoma colon cells. Resveratrol and resveratrol triacetate inhibit cell proliferation and arrest cell cycle. epsilon-Viniferin and epsilon-viniferin pentaacetate slightly reduce cell proliferation. Vineatrol inhibits cell proliferation and favors an accumulation in the S phase of the ce…

Cell Membrane Permeabilityendocrine system diseasesvineatrolMESH: Cell CycleMESH: DNA ReplicationMESH: Flow CytometryresveratrolResveratrolMESH : Antineoplastic Agents PhytogenicWine grapechemistry.chemical_compoundMESH: Structure-Activity RelationshipMESH: StilbenesStilbenesMESH : Structure-Activity RelationshipMESH: Cell Membrane Permeabilityskin and connective tissue diseasesfood and beveragesDNA NeoplasmMESH : Cell DivisionCell cycleFlow CytometryMESH : Colonic Neoplasmscolon cancerBiochemistryColonic NeoplasmsMESH: Cell Divisioncell cycleMESH : DNA NeoplasmCell Divisionhormones hormone substitutes and hormone antagonistsMESH : DNA ReplicationBiotechnologyDNA ReplicationMESH: XenobioticsMESH: Cell Line TumorMESH : Flow CytometryMESH: Antineoplastic Agents PhytogenicMESH: DNA NeoplasmMESH : XenobioticsBiologyXenobioticsMESH : StilbenesStructure-Activity RelationshipCell Line TumorMESH : Cell Cycle[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyHumansStructure–activity relationship[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologypolyphenolsS phaseMESH: Colonic NeoplasmsMESH: HumansMESH : Cell Line TumorCell growthorganic chemicalsMESH : HumansAntineoplastic Agents PhytogenicchemistryMESH : Cell Membrane PermeabilityAcetylationCell cultureCancer researchFood ScienceMolecular Nutrition & Food Research
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Colon Cancer Stem Cells: Promise of Targeted Therapy

2010

First developed for hematologic disorders, the concept of cancer stem cells (CSCs) was expanded to solid tumors, including colorectal cancer (CRC). The traditional model of colon carcinogenesis includes several steps that occur via mutational activation of oncogenes and inactivation of tumor suppressor genes. Intestinal epithelial cells exist for a shorter amount of time than that required to accumulate tumor-inducing genetic changes, so researchers have investigated the concept that CRC arises from the long-lived stem cells, rather than from the differentiated epithelial cells. Colon CSCs were originally identified through the expression of the CD133 glycoprotein using an antibody directed…

Cell SurvivalColonColorectal cancermedicine.medical_treatmentMetastasisTargeted therapyColon cancer stem cellsCancer stem cellBiomarkers TumormedicineAnimalsHumansHepatologybiologyCD44GastroenterologyLGR5Cell Differentiationmedicine.diseaseGene Expression Regulation NeoplasticCell Transformation NeoplasticDrug Resistance NeoplasmColonic NeoplasmsNeoplastic Stem CellsCancer researchbiology.proteinStem cellSignal TransductionAdult stem cell
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[Post-translational regulation of N-glycosylated proteins expression in human intestinal cells in culture].

1991

International audience; HT-29 cells derived from a human colonic adenocarcinoma, can express a typical intestinal differentiation. Undifferentiated HT-29 cells accumulate N-linked glycoproteins substituted with unprocessed carbohydrate chains before to degrade them. Conversely, carbohydrate chains of N-linked glycoproteins are classically processed in differentiated HT-29 cells. The instability of N-linked glycoproteins in undifferentiated HT-29 cells is due to their rapid delivery from the endoplasmic reticulum to a compartment with lysosomal characteristics. This catabolitic pathway involves a bypass of the Golgi apparatus.

Cell Transformation NeoplasticDrug StabilityLeupeptinsPolysaccharides[ CHIM.ORGA ] Chemical Sciences/Organic chemistry[CHIM.ORGA]Chemical Sciences/Organic chemistryColonic NeoplasmsTumor Cells CulturedHumansAdenocarcinoma[CHIM.ORGA] Chemical Sciences/Organic chemistryProtein Processing Post-TranslationalGlycoproteins
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