Search results for "Cromo"

showing 10 items of 1298 documents

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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Fascin upregulation in primary head and neck squamous cell carcinoma is associated with lymphatic metastasis

2014

Fascin is an actin-bundling protein that is associated with cellular motility and cancer-cell invasion. The present study aimed to examine the expression of fascin in head and neck squamous cell carcinoma (HNSCC) and its potential use as a biomarker. In a prospective study with a median follow-up time of 48.8 months, tumor tissues, adjacent healthy tissues and cervical lymph node metastases were collected from 25 patients and analyzed by immunohistochemistry. The specimens were scored according to the intensity of fascin staining and the percentage of tumor cells stained using a semi-quantitative scoring approach; the data were analyzed and correlated with clinical follow-up observations. A…

Cancer ResearchPathologymedicine.medical_specialtymacromolecular substancesfascinhead and neck squamous cell carcinomaMetastasislymphaticmedicinemetastasisLymph nodeFascinmarkerOncogenebiologybusiness.industryCancerArticlesmedicine.diseaseHead and neck squamous-cell carcinomaLymphatic systemmedicine.anatomical_structureOncologybiology.proteinImmunohistochemistrybusinessOncology Letters
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Ultrastructural evidence of collagenolytic activity in ductal infiltrating carcinoma of the human breast

1987

The stroma of ductal infiltrating carcinoma of the human breast shows characteristic and localized areas of collagen rarefaction and fragmentation. This finding has been correlated with a peculiar type of fibrillar damage, observed in a small percentage of collagen fibrils isolated in the native state from the tumour stroma. The same pattern of lesion has been reproduced in vitro by human collagenase digestion on reconstituted fibrils. No effect has been detected by other nonspecific proteases in the same system.

Cancer ResearchProteasesPathologymedicine.medical_specialtyMammary glandBreast Neoplasmsmacromolecular substancesBiologyLesionStromamedicineHumansTrypsinFragmentation (cell biology)AgedPancreatic ElastaseMiddle AgedIn vitroMicroscopy ElectronCarcinoma Intraductal NoninfiltratingMicrobial Collagenasemedicine.anatomical_structureOncologyCollagenaseUltrastructureFemaleCollagenmedicine.symptommedicine.drug
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Bmi1 and Cell of Origin Determinants of Brain Tumor Phenotype

2007

Glioblastomas frequently express oncogenic EGFR and loss of the Ink4a/Arf locus. Bmi1, a positive regulator of stem cell self renewal, may be critical to drive brain tumor growth. In this issue of Cancer Cell, Bruggeman and colleagues suggest that brain tumors with these molecular alterations can be initiated in both neural precursor and differentiated cell compartments in the absence of Bmi1; however, tumorigenicity is reduced, and tumors contain fewer precursor cells. Surprisingly, tumors appear less malignant when initiated in precursor cells. Bmi1-deficient tumors also had fewer neuronal lineage cells, suggesting a role for Bmi1 in determination of cell lineage and tumor phenotype.

Cancer ResearchTime FactorsCell of originCellular differentiationBrain tumormacromolecular substancesBiologyMiceProto-Oncogene ProteinsPrecursor cellmedicineAnimalsHumansCyclin-Dependent Kinase Inhibitor p16Cell ProliferationNeoplasm StagingMice KnockoutNeuronsPolycomb Repressive Complex 1Brain NeoplasmsCell growthStem CellsNuclear ProteinsCell DifferentiationNeoplasms ExperimentalCell Biologymedicine.diseaseStem Cell Self-RenewalErbB ReceptorsGene Expression Regulation NeoplasticRepressor ProteinsCell Transformation NeoplasticPhenotypeOncologyBMI1AstrocytesMutationCancer cellCancer researchGlioblastomaSignal TransductionCancer Cell
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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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cDNA sequences of the authentic keratins 8 and 18 in zebrafish

2003

From the zebrafish Danio rerio, we have cDNA cloned and sequenced a novel type II and a novel type I keratin, termed DreK8 and DreK18, respectively. We identified DreK8/18 as the true orthologs of the human keratin pair K8/18 as follows: (i) MALDI-MS assignment to the biochemically identified K8 and K18 candidates that are co-expressed in simple epithelia and absent in epidermal keratinocytes; (ii) multiple sequence alignments and phylogenetic tree analysis, showing that DreK8, within the phylogenetic tree of type II keratins, forms a highly bootstrap-supported branch together with K8 from goldfish and rainbow trout, whereas DreK18, within the phylogenetic tree of type I keratins, groups wi…

Cancer Researchanimal structuresType I keratinMolecular Sequence DataDaniomacromolecular substancesBiologyType II keratinComplementary DNAKeratinAnimalsHumansTissue DistributionAmino Acid SequenceCloning MolecularMolecular BiologyZebrafishPhylogenyZebrafishGeneticschemistry.chemical_classificationKeratin-18integumentary systemPhylogenetic treeKeratin-8Nucleic acid sequenceCell BiologyZebrafish Proteinsbiology.organism_classificationchemistryKeratinsSequence AlignmentDevelopmental BiologyDifferentiation
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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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Median progression free survival (PFS) for patients treated with everolimus (EVE) plus exemestane (EXE) for HR plus mBC in routine clinical practice …

2017

e12547 Background: BRAWO is a non-interventional study, which enrolled more than 2400 patients (pts) with advanced/metastatic, hormone-receptor-positive and HER2-negative breast cancer treated with EVE and EXE. Main objectives are a) the impact of physical activity on efficacy and quality of life, b) prophylaxis and management of stomatitis in clinical routine, and c) the sequence of therapy when EVE is used in daily clinical practice. We report updated data of the 3rd interim analysis, including PFS. Methods: This updated analysis (data cut-off 18 Oct 2016) covers data of the first 1345 documented pts with at least one follow up under therapy. Here we describe the baseline characteristics…

Cancer Researchmedicine.medical_specialtyEverolimusbusiness.industryMedizinmacromolecular substancesmedicine.diseaseInterim analysisSurgerystomatognathic diseaseschemistry.chemical_compoundBreast cancerOncologyQuality of lifeExemestanechemistryInternal medicineotorhinolaryngologic diseasesmedicineRoutine clinical practiceProgression-free survivalbusinessStomatitismedicine.drug
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A French prospective pilot study for identifying dihydropyrimidine dehydrogenase (DPD) deficiency in breast cancer patients (pts) receiving capecitab…

2013

e13519 Background: For fluoropyrimidines, and especially cap, Health Authorities point out that DPD deficiency confers a significant risk of major toxicity (tox). Identification of at-risk pts is thus relevant. This multicentric prospective study of the French GPCO group (Groupe de Pharmacologie Clinique Oncologique, Unicancer) evaluated the sensitivity, specificity and predictive values of DPD phenotyping and genotyping for predicting severe cap-related tox in metastatic breast cancer pts. Methods: 303 pts were included (15 institutions), 88% received cap as monotherapy, 28% were treated as first line (mean dose at 1st cycle 1957 mg/m2/d). Pre-treatment dihydrouracil (UH2) and uracil (U) …

Cancer Researchmedicine.medical_specialtymacromolecular substances030226 pharmacology & pharmacyGastroenterology[SPI.AUTO]Engineering Sciences [physics]/AutomaticCapecitabine03 medical and health scienceschemistry.chemical_compound0302 clinical medicineBreast cancerInternal medicine[ SPI.AUTO ] Engineering Sciences [physics]/AutomaticmedicineDihydropyrimidine dehydrogenaseProspective cohort studybusiness.industryDihydrouracilmedicine.diseaseMetastatic breast cancer3. Good healthSurgery[SPI.AUTO] Engineering Sciences [physics]/AutomaticOncologychemistry030220 oncology & carcinogenesisRelative riskToxicitybacteriaPublished in Journal of Clinical Oncology vol. 31 : 2013 (Suppl ;abstr e13519)businessmedicine.drug
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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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