Search results for "Xenograft"

showing 10 items of 161 documents

Natural polyphenols facilitate elimination of HT-29 colorectal cancer xenografts by chemoradiotherapy: a Bcl-2- and superoxide dismutase 2-dependent …

2008

AbstractColorectal cancer is one of the most common malignancies worldwide. The treatment of advanced colorectal cancer with chemotherapy and radiation has two major problems: development of tumor resistance to therapy and nonspecific toxicity towards normal tissues. Different plant-derived polyphenols show anticancer properties and are pharmacologically safe. In vitro growth of human HT-29 colorectal cancer cells is inhibited (∼56%) by bioavailable concentrations of trans-pterostilbene (trans-3,5-dimethoxy-4′-hydroxystilbene; t-PTER) and quercetin (3,3′,4′,5,6-pentahydroxyflavone; QUER), two structurally related and naturally occurring small polyphenols. I.v. administration of t-PTER and Q…

Cancer ResearchAntioxidantColorectal cancerSp1 Transcription Factormedicine.medical_treatmentDown-RegulationMice NudeAntineoplastic AgentsBiologyAntioxidantsSuperoxide dismutaseMicePhenolsIn vivoGene expressionmedicineAnimalsHumansCell ProliferationFlavonoidsChemotherapySuperoxide DismutaseGene Expression ProfilingNF-kappa BPolyphenolsmedicine.diseaseChemotherapy regimenXenograft Model Antitumor AssaysOxaliplatinUp-RegulationOncologyBiochemistryProto-Oncogene Proteins c-bcl-2Drug Resistance NeoplasmCancer researchbiology.proteinFemaleColorectal NeoplasmsHT29 Cellsmedicine.drugMolecular cancer therapeutics
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Application of patient-derived liver cancer cells for phenotypic characterization and therapeutic target identification.

2018

Primary liver cancer (PLC) ranks among the most lethal solid cancers worldwide due to lack of effective biomarkers for early detection and limited treatment options in advanced stages. Development of primary culture models that closely recapitulate phenotypic and molecular diversities of PLC is urgently needed to improve the patient outcome. Long-term cultures of 7 primary liver cancer cell lines of hepatocellular and cholangiocellular origin were established using defined culture conditions. Morphological and histological characteristics of obtained cell lines and xenograft tumors were analyzed and compared to original tumors. Time course analyses of transcriptomic and genomic changes were…

Cancer ResearchCarcinogenesisDNA Mutational AnalysisPrimary Cell CultureAntineoplastic AgentsDiseaseBiologymedicine.disease_causeTranscriptome03 medical and health sciencesMice0302 clinical medicineCell Line TumormedicineBiomarkers TumorAnimalsHumansPrecision MedicineDrug discoveryGene Expression ProfilingLiver NeoplasmsHigh-Throughput Nucleotide SequencingGenomicsPrecision medicinemedicine.diseasePhenotypeXenograft Model Antitumor AssaysOncologyCell culture030220 oncology & carcinogenesisMutationCancer researchKRASLiver cancerInternational journal of cancer
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The human Lgl polarity gene, Hugl-2, induces MET and suppresses Snail tumorigenesis

2012

Lethal giant larvae proteins have key roles in regulating polarity in a variety of cell types and function as tumour suppressors. A transcriptional programme initiated by aberrant Snail expression transforms epithelial cells to potentially aggressive cancer cells. Although progress in defining the molecular determinants of this programme has been made, we have little knowledge as to how the Snail-induced phenotype can be suppressed. In our studies we identified the human lethal giant larvae homologue 2, Hugl-2, (Llgl2/Lgl2) polarity gene as downregulated by Snail. Snail binds E-boxes in the Hugl-2 promoter and represses Hugl-2 expression, whereas removal of the E-boxes releases Hugl-2 from …

Cancer ResearchCell typeMice SCIDSnailmedicine.disease_causeMiceMice Inbred NODbiology.animalChlorocebus aethiopsparasitic diseasesCell polarityGeneticsmedicineAnimalsHumansGenes Tumor SuppressorNeoplasm MetastasisMolecular BiologyTranscription factorCells CulturedRegulation of gene expressionbiologyfungiHEK 293 cellsCell PolarityHep G2 CellsAnatomyProto-Oncogene Proteins c-metXenograft Model Antitumor AssaysPhenotypeUp-RegulationCell biologyGene Expression Regulation NeoplasticCytoskeletal ProteinsCell Transformation NeoplasticHEK293 CellsCOS CellsSnail Family Transcription FactorsCarcinogenesisProtein BindingTranscription FactorsOncogene
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Moguntinones--new selective inhibitors for the treatment of human colorectal cancer.

2014

Abstract 3-Indolyl and 3-azaindolyl-4-aryl maleimide derivatives, called moguntinones (MOG), have been selected for their ability to inhibit protein kinases associated with angiogenesis and induce apoptosis. Here, we characterize their mode of action and their potential clinical value in human colorectal cancer in vitro and in vivo. MOG-19 and MOG-13 were characterized in vitro using kinase, viability, and apoptosis assays in different human colon cancer (HT-29, HCT-116, Caco-2, and SW480) and normal colon cell lines (CCD-18Co, FHC, and HCoEpiC) alone or in combination with topoisomerase I inhibitors. Intracellular signaling pathways were analyzed by Western blotting. To determine their pot…

Cancer ResearchIndolesColorectal cancerAngiogenesisApoptosisBiologyPharmacologyMetastasisMaleimidesMiceIn vivomedicineAnimalsHumansPI3K/AKT/mTOR pathwayKinaseTOR Serine-Threonine Kinasesmedicine.diseaseXenograft Model Antitumor AssaysOncologyApoptosisSignal transductionCaco-2 CellsTopoisomerase I InhibitorsColorectal NeoplasmsHT29 CellsProto-Oncogene Proteins c-aktSignal TransductionMolecular cancer therapeutics
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β-Catenin Contributes to Lung Tumor Development Induced by EGFR Mutations

2014

Abstract The discovery of somatic mutations in EGFR and development of EGFR tyrosine kinase inhibitors (TKI) have revolutionized treatment for lung cancer. However, resistance to TKIs emerges in almost all patients and currently no effective treatment is available. Here, we show that β-catenin is essential for development of EGFR-mutated lung cancers. β-Catenin was upregulated and activated in EGFR-mutated cells. Mutant EGFR preferentially bound to and tyrosine phosphorylated β-catenin, leading to an increase in β-catenin–mediated transactivation, particularly in cells harboring the gefitinib/erlotinib-resistant gatekeeper EGFR-T790M mutation. Pharmacologic inhibition of β-catenin suppresse…

Cancer ResearchLung NeoplasmsCarcinogenesisAfatinibMutation MissenseAntineoplastic AgentsMice TransgenicAfatinibmedicine.disease_causeArticleTransactivationGefitinibCarcinoma Non-Small-Cell LungCell Line TumormedicineAnimalsHumansEpidermal growth factor receptorLung cancerbeta CateninMutationbiologyProtein Stabilitymedicine.diseaseXenograft Model Antitumor AssaysTumor BurdenUp-Regulationrespiratory tract diseasesErbB ReceptorsGene Expression Regulation NeoplasticHEK293 CellsOncologyDoxycyclineCateninImmunologyQuinazolinesCancer researchbiology.proteinCarcinogenesismedicine.drugCancer Research
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Targeting transcriptional addictions in small cell lung cancer with a covalent CDK7 inhibitor.

2014

Small cell lung cancer (SCLC) is an aggressive disease with high mortality, and the identification of effective pharmacological strategies to target SCLC biology represents an urgent need. Using a high-throughput cellular screen of a diverse chemical library, we observe that SCLC is sensitive to transcription-targeting drugs, in particular to THZ1, a recently identified covalent inhibitor of cyclin-dependent kinase 7. We find that expression of super-enhancer-associated transcription factor genes, including MYC family proto-oncogenes and neuroendocrine lineage-specific factors, is highly vulnerability to THZ1 treatment. We propose that downregulation of these transcription factors contribut…

Cancer ResearchLung NeoplasmsTranscription GeneticMolecular Sequence DataAntineoplastic AgentsBiologyBioinformaticsArticleMiceSuper-enhancerDownregulation and upregulationCell Line TumorMedicineAnimalsHumansEnzyme InhibitorsneoplasmsTranscription factorRegulation of gene expressionbusiness.industryCell BiologyNeoplasms ExperimentalSequence Analysis DNASmall Cell Lung CarcinomaXenograft Model Antitumor AssayshumanitiesCyclin-Dependent Kinasesrespiratory tract diseasesHigh-Throughput Screening AssaysGene Expression Regulation NeoplasticOncologyCovalent bondCancer cellCancer researchNon small cellSmall Cell Lung CarcinomaCyclin-dependent kinase 7businessTranscription Factor GeneCDK12Transcription FactorsCancer cell
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Multivalent DR5 peptides activate the TRAIL death pathway and exert tumoricidal activity.

2010

Abstract Ongoing clinical trials are exploring anticancer approaches based on signaling by TRAIL, a ligand for the cell death receptors DR4 and DR5. In this study, we report on the selective apoptotic effects of multivalent DR5 binding peptides (TRAILmim/DR5) on cancer cells in vitro and in vivo. Surface plasmon resonance revealed up to several thousand-fold increased affinities of TRAILmim/DR5-receptor complexes on generation of divalent and trivalent molecules, the latter of which was achieved with a conformationally restricted adamantane core. Notably, only multivalent molecules triggered a substantial DR5-dependent apoptotic response in vitro. In tumor models derived from human embryoni…

Cancer ResearchMembrane transport and intracellular motility [NCMLS 5]Apoptosis[CHIM.THER]Chemical Sciences/Medicinal Chemistry[ SDV.CAN ] Life Sciences [q-bio]/CancerTNF-Related Apoptosis-Inducing LigandMice0302 clinical medicineStilbenesReceptorCells Cultured0303 health sciencesDrug Synergism[ CHIM.THER ] Chemical Sciences/Medicinal ChemistryLigand (biochemistry)Tumor Burden3. Good healthMitochondrial medicine [IGMD 8]Oncology030220 oncology & carcinogenesisColonic NeoplasmsFemaleOligopeptidesSignal Transductionmedicine.medical_specialtyProgrammed cell deathBlotting WesternMolecular Sequence DataMice Nude[SDV.CAN]Life Sciences [q-bio]/CancerCell Line03 medical and health sciencesIn vivoInternal medicinemedicineAnimalsHumansAmino Acid Sequence030304 developmental biologybusiness.industrySurface Plasmon ResonanceHCT116 CellsAntineoplastic Agents PhytogenicXenograft Model Antitumor AssaysIn vitroReceptors TNF-Related Apoptosis-Inducing LigandEndocrinologyResveratrolCell cultureApoptosisCancer cellCancer researchbusiness
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Nanofitins targeting heat shock protein 110: an innovative immunotherapeutic modality in cancer.

2021

The presence of an inactivating heat shock protein 110 (HSP110) mutation in colorectal cancers has been correlated with an excellent prognosis and with the ability of HSP110 to favor the formation of tolerogenic (M2-like) macrophages. These clinical and experimental results suggest a potentially powerful new strategy against colorectal cancer: the inhibition of HSP110. In this work, as an alternative to neutralizing antibodies, Nanofitins (scaffold ~7 kDa proteins) targeting HSP110 were isolated from the screening of a synthetic Nanofitin library, and their capacity to bind (immunoprecipitation, biolayer interferometry) and to inhibit HSP110 was analyzed in vitro and in vivo. Three Nanofiti…

Cancer ResearchMice03 medical and health sciencesLymphocytes Tumor-Infiltrating0302 clinical medicineImmune systemPeptide LibraryIn vivoCell Line TumorHeat shock proteinTumor MicroenvironmentmedicineAnimalsHumansCytotoxic T cellHSP110 Heat-Shock Proteinssmall peptide moleculesTumor microenvironmentanticancer targeted therapybiologyChemistryMacrophagesCancer[SDV.SP]Life Sciences [q-bio]/Pharmaceutical sciencesmedicine.diseaseXenograft Model Antitumor AssaysPeptide FragmentsIn vitro3. Good healthNanofitinsOncologyPositron-Emission Tomography030220 oncology & carcinogenesisbiology.proteinCancer researchFemaleAntibodyColorectal NeoplasmsHSP110
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The dual PI3K/mTOR inhibitor PKI-587 enhances sensitivity to cetuximab in EGFR-resistant human head and neck cancer models

2014

Background:Cetuximab is the only targeted agent approved for the treatment of head and neck squamous cell carcinomas (HNSCC), but low response rates and disease progression are frequently reported. As the phosphoinositide 3-kinase (PI3K) and the mammalian target of rapamycin (mTOR) pathways have an important role in the pathogenesis of HNSCC, we investigated their involvement in cetuximab resistance.Methods:Different human squamous cancer cell lines sensitive or resistant to cetuximab were tested for the dual PI3K/mTOR inhibitor PF-05212384 (PKI-587), alone and in combination, both in vitro and in vivo.Results:Treatment with PKI-587 enhances sensitivity to cetuximab in vitro, even in the co…

Cancer ResearchPathologyCetuximabApoptosisHNSCCHNSCCMiceAntineoplastic Combined Chemotherapy ProtocolsNeoplasmPhosphoinositide-3 Kinase InhibitorsMice Inbred BALB CCetuximabCaspase 3TriazinesTOR Serine-Threonine KinasesCetuximab resistanceErbB ReceptorsOncologyHead and Neck NeoplasmsMonoclonalCarcinoma Squamous Cellmedicine.drugmedicine.medical_specialtyMorpholinesPI3K-mTOR inhibitorsMice NudeAntineoplastic AgentsBiologyAntibodies Monoclonal HumanizedCell Line TumorAutophagymedicineCarcinomaAnimalsHumansneoplasmsPI3K/AKT/mTOR pathwayCell Proliferationcetuximab resistanceSquamous Cell Carcinoma of Head and Necktarget therapyCell growthAutophagyCancermedicine.diseaseXenograft Model Antitumor Assaysdigestive system diseasesDrug Resistance NeoplasmPI3K7mTOR inhibitorsCancer researchTranslational TherapeuticsBritish Journal of Cancer
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Evidence for characteristic vascular patterns in solid tumours: quantitative studies using corrosion casts

1999

The vascular architecture of four different tumour cell lines (CaX, CaNT, SaS, HEC-1B) transplanted subcutaneously in mice was examined by means of microvascular corrosion casting in order to determine whether there is a characteristic vascular pattern for different tumour types and whether it differs significantly from two normal tissues, muscle and gut. Three-dimensional reconstructed scanning electron microscope images were used for quantitative measurements. Vessel diameters, intervessel and interbranch distances showed large differences between tumour types, whereas the branching angles were similar. In all tumours, the variability of the vessel diameters was significantly higher than …

Cancer ResearchPathologymedicine.medical_specialtyAngiogenesisTransplantation Heterologousvascular patternNormal tissueMice NudeAdenocarcinomaBiologyCorrosion CastingVascular architectureMiceMicroscopyTumor Cells CulturedmedicineAnimalsHumansmicrovascular corrosion castingtumourCarcinomaRegular ArticleNeoplasms ExperimentalAnatomymedicine.diseaseEndometrial NeoplasmsTransplantationxenograftsOncologyVascular networkrodentsMice Inbred CBAMicroscopy Electron ScanningFemaleSarcoma ExperimentalSarcomaCorrosion CastingNeoplasm TransplantationBritish Journal of Cancer
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