Search results for "SUBSTANCES"

showing 10 items of 1122 documents

Mechanisms of environmental chemicals that enable the cancer hallmark of evasion of growth suppression

2015

As part of the Halifax Project, this review brings attention to the potential effects of environmental chemicals on important molecular and cellular regulators of the cancer hallmark of evading growth suppression. Specifically, we review the mechanisms by which cancer cells escape the growth-inhibitory signals of p53, retinoblastoma protein, transforming growth factor-beta, gap junctions and contact inhibition. We discuss the effects of selected environmental chemicals on these mechanisms of growth inhibition and cross-reference the effects of these chemicals in other classical cancer hallmarks.

Cancer ResearchReviewHazardous Substanceschemistry.chemical_compoundNeoplasmsAnimalsHumansMedicinebiologyAnimalbusiness.industryMedicine (all)Retinoblastoma proteinContact inhibitionCancerEnvironmental ExposureGeneral MedicineEnvironmental exposureEvasion (ethics)medicine.diseaseCell biologychemistryHazardous SubstanceImmunologyCancer cellbiology.proteinNeoplasmSignal transductionGrowth inhibitionbusinessHumanSignal TransductionCarcinogenesis
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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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Knockout of thep-Coumarate Decarboxylase Gene fromLactobacillus plantarumReveals the Existence of Two Other Inducible Enzymatic Activities Involved i…

2000

ABSTRACTLactobacillus plantarumNC8 contains apdcgene coding forp-coumaric acid decarboxylase activity (PDC). A food grade mutant, designated LPD1, in which the chromosomalpdcgene was replaced with the deletedpdcgene copy, was obtained by a two-step homologous recombination process using an unstable replicative vector. The LPD1 mutant strain remained able to weakly metabolizep-coumaric and ferulic acids into vinyl derivatives or into substituted phenyl propionic acids. We have shown thatL. plantarumhas a second acid phenol decarboxylase enzyme, better induced with ferulic acid than withp-coumaric acid, which also displays inducible acid phenol reductase activity that is mostly active when gl…

Carboxy-lyasesCoumaric AcidsCarboxy-LyasesMutantGenetics and Molecular Biologymacromolecular substancesCoumaric acidApplied Microbiology and BiotechnologyFerulic acidchemistry.chemical_compoundHydroxybenzoatesCloning Molecularchemistry.chemical_classificationEcologybiologyhemic and immune systemsMetabolismPhenolic acidHydrogen-Ion Concentrationbiology.organism_classificationLactobacillusElectroporationEnzymechemistryBiochemistryEnzyme InductionPropionatesOxidoreductasesGene DeletionLactobacillus plantarumFood ScienceBiotechnologyApplied and Environmental Microbiology
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Human Embryonic Stem Cell Derived Hepatocyte-Like Cells as a Tool for In Vitro Hazard Assessment of Chemical Carcinogenicity

2011

Hepatocyte-like cells derived from the differentiation of human embryonic stem cells (hES-Hep) have potential to provide a human relevant in vitro test system in which to evaluate the carcinogenic hazard of chemicals. In this study, we have investigated this potential using a panel of 15 chemicals classified as noncarcinogens, genotoxic carcinogens, and nongenotoxic carcinogens and measured whole-genome transcriptome responses with gene expression microarrays. We applied an ANOVA model that identified 592 genes highly discriminative for the panel of chemicals. Supervised classification with these genes achieved a cross-validation accuracy of > 95%. Moreover, the expression of the response g…

Carcinogenicity TestsCellular differentiationCell Culture TechniquesGene Expressionsystems toxicologyComputational biologyBiologyToxicologymedicine.disease_causeHazardous SubstancesTranscriptomecomputational biologyCytochrome P-450 Enzyme SystemNaturvetenskapmedicinecarcinogenicityHumansMicroscopy Phase-ContrastEmbryonic Stem CellsCarcinogenAnalysis of VarianceDose-Response Relationship DrugReverse Transcriptase Polymerase Chain ReactionMicroarray analysis techniquesGene Expression ProfilingReproducibility of Resultsrisk assessmentCell DifferentiationMicroarray AnalysisImmunohistochemistryEmbryonic stem cellMolecular biologyGene expression profilingCell culturetoxicogenomicsCarcinogensHepatocytesNatural SciencesCarcinogenesisToxicological Sciences
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Deleting Full Length Titin Versus the Titin M-Band Region Leads to Differential Mechanosignaling and Cardiac Phenotypes

2019

Background: Titin is a giant elastic protein that spans the half-sarcomere from Z-disk to M-band. It acts as a molecular spring and mechanosensor and has been linked to striated muscle disease. The pathways that govern titin-dependent cardiac growth and contribute to disease are diverse and difficult to dissect. Methods: To study titin deficiency versus dysfunction, the authors generated and compared striated muscle specific knockouts (KOs) with progressive postnatal loss of the complete titin protein by removing exon 2 (E2-KO) or an M-band truncation that eliminates proper sarcomeric integration, but retains all other functional domains (M-band exon 1/2 [M1/2]-KO). The authors evaluated c…

Cardiomyopathy DilatedMaleSarcomeresanimal structuresVentricular Dysfunction Rightmacromolecular substances030204 cardiovascular system & hematologyMechanotransduction CellularVentricular Function LeftArticleMuscle hypertrophyVentricular Dysfunction Left03 medical and health sciences0302 clinical medicinePhysiology (medical)AnimalsMedicineMyocytes CardiacMuscle Skeletal030304 developmental biologyMice Knockout0303 health sciencesbiologybusiness.industryMolecular springmusculoskeletal systemPhenotypeCell biologyMuscular AtrophyPhenotypeMuscle diseasecardiovascular systemVentricular Function Rightbiology.proteinTitinCardiology and Cardiovascular MedicinebusinessProtein KinasesGene DeletionDifferential (mathematics)Circulation
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