Search results for "Carbohydrate"

showing 10 items of 882 documents

Impact of Extracellular Acidity on the Activity of P-glycoprotein and the Cytotoxicity of Chemotherapeutic Drugs

2006

AbstractThe expression and activity of P-glycoprotein (pGP) play a role in the multidrug resistance of tumors. Because solid-growing tumors often show pronounced hypoxia or extracellular acidosis, this study attempted to analyze the impact of an acidic environment on the expression and activity of pGP and on the cytotoxicity of chemotherapeutic agents. For this, prostate carcinoma cells were exposed to an acidic extracellular environment (pH 6.6) for up to 24 hours. pGP activity was more than doubled after 3 to 6 hours of incubation in acidic medium, whereas cellular pGP expression remained constant, indicating that increased transport rate is the result of functional modulation. In paralle…

Cancer ResearchDaunorubicinPharmacologyP-glycoproteinlcsh:RC254-282Calcium in biologyExtracellularmedicinepolycyclic compoundsintracellular Ca2+ concentrationCytotoxicityacidityProtein kinase CP-glycoproteinbiologyintegumentary systemChemistrychemotoxicitylcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogenscarbohydrates (lipids)BiochemistryCell culturebiology.proteinIntracellularmedicine.drugprotein kinase CNeoplasia
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The AC133 epitope, but not the CD133 protein, is lost upon cancer stem cell differentiation.

2010

Abstract Colon cancer stem cells (CSC) can be identified with AC133, an antibody that detects an epitope on CD133. However, recent evidence suggests that expression of CD133 is not restricted to CSCs, but is also expressed on differentiated tumor cells. Intriguingly, we observed that detection of the AC133 epitope on the cell surface decreased upon differentiation of CSC in a manner that correlated with loss of clonogenicity. However, this event did not coincide with a change in CD133 promoter activity, mRNA, splice variant, protein expression, or even cell surface expression of CD133. In contrast, we noted that with CSC differentiation, a change occured in CD133 glycosylation. Thus, AC133 …

Cancer ResearchGlycosylationGlycosylationCellular differentiationCellAC 133 EpitopeDown-RegulationMice SCIDEpitopechemistry.chemical_compoundEpitopesMiceCancer stem cellAntigens CDMice Inbred NODProminin-1medicineTumor Cells CulturedAnimalsHumansProtein IsoformsAC133 AntigenRNA MessengerPromoter Regions GeneticneoplasmsGlycoproteinsbiologyCell DifferentiationMolecular biologycarbohydrates (lipids)Gene Expression Regulation Neoplasticmedicine.anatomical_structureOncologychemistryembryonic structuresColonic Neoplasmsbiology.proteinNeoplastic Stem CellsAntibodyStem cellPeptidesCancer research
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Inhibition of human immunodeficiency virus-1 infection by human conglutinin-like protein: in vitro studies.

1992

The lectin-like protein analogous to bovine conglutinin was purified from human serum. The carbohydrate-binding ability of conglutinin-like protein was inhibited by D-mannose, N-acetylglucosamine and L-fucose as well as by mannan-containing oligosaccharides. By applying a lectin-based ELISA system it was demonstrated that conglutinin-like protein binds to human immunodeficiency virus-1 (HIV-1) glycoprotein 120 (gp120) via its carbohydrate binding site. In vitro experiments with T-lymphoblastoid CEM cells revealed that conglutinin-like protein abolishes infection by HIV-1; a 50% cytoprotective concentration of 23.9 micrograms/ml was measured. These findings demonstrate that human conglutinin…

Cancer ResearchMolecular Sequence DataCarbohydratesImmunoglobulinsEnzyme-Linked Immunosorbent AssayHIV Envelope Protein gp120Mannose-Binding LectinVirusChromatography AffinityArticleViral ProteinsConglutininProtein A/GHumansImmunoconglutininsBinding siteKey wordsConglutinin‐like proteinchemistry.chemical_classificationAcquired Immunodeficiency SyndromebiologyHIV‐1Immunization PassiveLectinMolecular biologyMannanIn vitrogp120OncologychemistryCarbohydrate Sequencebiology.proteinHIV-1Protein GGlycoproteinCarrier ProteinsLectinJapanese journal of cancer research : Gann
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Establishment of a [18F]-FDG-PET/MRI Imaging Protocol for Gastric Cancer PDX as a Preclinical Research Tool

2020

Purpose The utility of 18-fluordesoxyglucose positron emission tomography ([18F]-FDG-PET) combined with computer tomography or magnetic resonance imaging (MRI) in gastric cancer remains controversial and a rationale for patient selection is desired. This study aims to establish a preclinical patient-derived xenograft (PDX) based [18F]-FDG-PET/MRI protocol for gastric cancer and compare different PDX models regarding tumor growth and FDG uptake. Materials and methods Female BALB/c nu/nu mice were implanted orthotopically and subcutaneously with gastric cancer PDX. [18F]-FDG-PET/MRI scanning protocol evaluation included different tumor sizes, FDG doses, scanning intervals, and organ-specific …

Cancer ResearchPathologymedicine.medical_specialtyStandardized uptake value03 medical and health sciences0302 clinical medicinemedicineAviditymedicine.diagnostic_testbiologybusiness.industryXenograftGastroenterologyGlucose transporterCancerMagnetic resonance imagingPET scanmedicine.diseasecarbohydrates (lipids)OncologyPositron emission tomography030220 oncology & carcinogenesisbiology.proteinImmunohistochemistry030211 gastroenterology & hepatologyGLUT1Original ArticlebusinessGastric cancerGlycolysisJournal of Gastric Cancer
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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
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Effects of interferon gamma on the proliferation and modulation of cell-surface structures of human ovarian carcinoma cell lines.

1993

Platinum-containing regimens are very effective in the primary treatment of ovarian cancer. However, upon subsequent treatment most tumors develop multidrug resistance. The clinical application of biological response modifiers like interferon gamma (IFN gamma) in advanced ovarian cancer is therefore of increasing interest. Permanent ovarian cancer cell lines are suitable for investigating the mode of action and the potential clinical effectiveness of such response modifiers. IFN gamma is known to modulate many cellular functions. In this study it was compared for its antiproliferative and antigen-modulatory activity on the expression of tumor-associated (CA-125, HMFG, CEA) and major histoco…

Cancer ResearchReceptor expressionCellInterferon-gammaAntigenEpidermal growth factorAntigens NeoplasmHLA AntigensMHC class ImedicineTumor Cells CulturedHumansAntigens Tumor-Associated CarbohydrateOvarian NeoplasmsMHC class IIbiologyCell growthCell MembraneGeneral Medicinemedicine.diseaseRecombinant ProteinsErbB ReceptorsGene Expression Regulation Neoplasticmedicine.anatomical_structureOncologyImmunologyAntigens Surfacebiology.proteinCancer researchFemaleOvarian cancerCell DivisionJournal of cancer research and clinical oncology
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pRb2/p130-E2F4/5-HDAC1-SUV39H1-p300 and pRb2/p130-E2F4/5-HDAC1-SUV39H1-DNMT1 multimolecular complexes mediate the transcription of estrogen receptor-…

2003

The estrogen receptor-alpha (ER) plays a crucial role in normal breast development and is also linked to development and progression of mammary carcinoma. The transcriptional repression of ER-alpha gene in breast cancer is an area of active investigation with potential clinical significance. However, the molecular mechanisms that regulate the ER-alpha gene expression are not fully understood. Here we show a new molecular mechanism of ER-alpha gene inactivation mediated by pRb2/p130 in ER-negative breast cancer cells. We investigated in vivo occupancy of ER-alpha promoter by pRb2/p130-E2F4/5-HDAC1-SUV39 H1-p300 and pRb2/p130-E2F4/5-HDAC1-SUV39H1-DNMT1 complexes, and provided a link between p…

Cancer ResearchTranscription GeneticEstrogen receptorHistone Deacetylase 1HistonesTumor Cells CulturedDNA (Cytosine-5-)-MethyltransferasesReceptorPromoter Regions GeneticE2F4Nuclear ProteinsAcetylationChromatinDNA-Binding ProteinsGene Expression Regulation NeoplasticReceptors Estrogenembryonic structuresDNA methylationFemalepRb2/p130; chromatin-modifying enzymes; estrogen receptor-alpha; breast carcinomabiological phenomena cell phenomena and immunityDNA (Cytosine-5-)-Methyltransferase 1medicine.medical_specialtyanimal structuresmedicine.drug_classMacromolecular SubstancesBreast NeoplasmsE2F4 Transcription FactorBiologyHistone DeacetylasesBreast cancerInternal medicineGeneticsmedicineEstrogen Receptor betaHumansMolecular BiologyEstrogen receptor betaE2F5 Transcription FactorRetinoblastoma-Like Protein p130Estrogen Receptor alphaProteinsMethyltransferasesDNA Methylationmedicine.diseasePhosphoproteinsRepressor Proteinsenzymes and coenzymes (carbohydrates)EndocrinologyEstrogenCancer researchTrans-ActivatorsEstrogen receptor alphaTranscription FactorsOncogene
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AURKA (aurora kinase A)

2011

Review on AURKA (aurora kinase A), with data on DNA, on the protein encoded, and where the gene is implicated.

Cancer Researchmacromolecular substancesHematologyBiologyCell biologySettore BIO/18 - Geneticaenzymes and coenzymes (carbohydrates)chemistry.chemical_compoundOncologychemistryembryonic structuresGeneticsAurora Kinase Abiological phenomena cell phenomena and immunityAURK-AGeneDNAAtlas of Genetics and Cytogenetics in Oncology and Haematology
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?(1,3)Fucosyltransferase expression in E-selectin-mediated binding of gastrointestinal tumor cells

1996

E-selectin recognizes the oncofetal antigen sialyl-Lewis X, which is highly expressed in adenocarcinoma. Five α(1,3)fucosyltransferases (FT) have been cloned that confer cell-surface expression of sialyl-Lewis X on transfected cells. We show here that 12/18 gastrointestinal-tumor cell lines bind specifically to immobilized E-selectin and that in sialyl-Lewis-X-positive cells binding is inhibited with a monoclonal antibody against sialyl-Lewis X. Using RT-PCR, we determined the expression of the α(1,3)fucosyltransferases III, IV, V, VI and VII in gastrointestinal tumor cells. Transcripts of FT IV and FT VII are abundantly expressed in all tested cells. Therefore no single fucosyltransferase …

Cancer Researchmedicine.medical_specialtyFucosyltransferasebiologyCell adhesion moleculemedicine.drug_classTransfectionMonoclonal antibodyMolecular biologycarbohydrates (lipids)FucosyltransferasesEndocrinologyOncologyCell cultureInternal medicineE-selectinmedicinebiology.proteinOncofetal antigenInternational Journal of Cancer
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Droloxifene-Induced Spikes of Tumor Markers Predict Benefit of Therapy

1991

In the clinical monitoring of cancer, tumor marker proteins may reflect the status of the disease. In cases with radio- and chemotherapy, spikes of tumor markers were found shortly after starting the therapy. These spikes were interpreted as a sign of tumor lysis. Recently during therapy of breast cancer with the new antiestrogen droloxifene, spikes of CA 125 and CA 15-3 were also found in about one-third of patients responding to therapy. The peaks of these initial increases were recorded between 14 and 60 days after the onset of treatment, with maximum concentrations up to 1,890% of the initial value. Marker concentrations decreased thereafter, to new baselines at or below the initial val…

Cancer Researchmedicine.medical_treatmentRadioimmunoassayAntineoplastic AgentsBreast NeoplasmsBreast cancerPredictive Value of TestsmedicineHumansAntigens Tumor-Associated CarbohydrateAgedTumor markerChemotherapybusiness.industryEstrogen AntagonistsCancerRadioimmunoassayMiddle Agedmedicine.diseaseAntiestrogenTamoxifenTreatment OutcomeOncologyPredictive value of testsCancer researchDrug EvaluationFemalebusinessTamoxifenmedicine.drugAmerican Journal of Clinical Oncology
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