Search results for " Neoplastic"

showing 10 items of 662 documents

Morphological transformation and DNA adduct formation by dibenz[a,h]anthracene and its metabolites in C3H10T1/2CL8 cells.

1994

The major routes of metabolic activation of dibenz[a,h]-anthracene (DBA) have been studied in transformable C3H10T1/2CL8 (C3H10T1/2) mouse embryo fibroblasts in culture. The morphological transforming activities of three potential intermediates formed by metabolism of DBA by C3H10T1/2 cells, trans-3,4-dihydroxy-3,4-dihydro-DBA-(DBA-3,4-diol), trans-dihydroxy-3,4-dihydro-DBA-anti-1,2-oxide (DBA-3,4-diol-1,2-oxide) and DBA-5,6-oxide were determined. DBA-3,4-diol-1,2-oxide was a strong morphological transforming agent giving a mean of 73% dishes with Type II or III foci and 1.63 Type II and III foci per dish at 0.5 microgram/ml. DBA-3,4-diol produced a mean of 42% dishes with Type II or III fo…

Cancer ResearchBiologychemistry.chemical_compoundDNA AdductsMiceStructure-Activity Relationshippolycyclic compoundsmedicineBenz(a)AnthracenesDeoxyguanosineDibenz(ah)anthraceneAnimalsFibroblastCarcinogenBiotransformationMice Inbred C3HGeneral MedicineMetabolismFibroblastsIn vitromedicine.anatomical_structureCell Transformation NeoplasticchemistryBiochemistryCell cultureIsotope LabelingOxidation-ReductionPhosphorus RadioisotopesDNACarcinogenesis
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Oral microbiome in Proliferative Verrucous Leukoplakia exhibits loss of diversity and enrichment of pathogens.

2021

Abstract Objectives Oral microbiome plays an important role in oral diseases. Among them, proliferative verrucous leucoplakia (PVL) is an uncommon form of progressive multifocal leukoplakia with a worryingly rate of malignant transformation. Here, we aimed to characterize the oral microbiome of PVL patients and compare it with those of healthy controls. Material and methods Oral biopsies from ten PVL patients and five healthy individuals were obtained and used to compare their microbial communities. The sequence of the V3-V4 region of 16S rRNA gene was used as the taxonomic basis to estimate and analyze the composition and diversity of bacterial populations present in the samples. Results O…

Cancer ResearchBiopsymedicine.disease_causeCampylobacter jejuniRNA Ribosomal 16SmedicineProliferative verrucous leukoplakiaHumansEubacteriumLeukoplakiaMouthbiologyCampylobacterMicrobiotabiochemical phenomena metabolism and nutritionrespiratory systembacterial infections and mycosesbiology.organism_classificationmedicine.disease16S ribosomal RNAstomatognathic diseasesCell Transformation NeoplasticOncologyImmunologyOral MicrobiomeOral SurgeryLeukoplakia OralDysbiosisOral oncology
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Expression of the IAPs in multidrug resistant tumor cells

2003

We have investigated the expression of the IAPs (inhibitory of apoptosis proteins) in the human HL-60 leukemia and in its multidrug resistant, P-glycoprotein (P-gp) over-expressing variant, HL-60R. HL-60R exhibits resistance to apoptosis induced from P-gp substrate drugs and also from other triggers (cisplatin, TNF-alpha, Fas ligation, TRAIL, IFN-gamma and serum starvation) not related to the multidrug transporter. Except for c-IAP-1 mRNA, HL-60R significantly over-expressed both the mRNAs and the proteins of all the IAPs studied, i.e. c-IAP-1, c-IAP-2, XIAP, NAIP and survivin. Determination of the DNA-binding capacity of NF-kappaB (p50 or p65 subunits) indicated that, while HL-60 cells sho…

Cancer ResearchBlotting WesternCellApoptosisHL-60 CellsBiologyInhibitor of Apoptosis Proteinsmultidrug resistanceSurvivinmedicineHumansRNA MessengerCisplatinOncogeneReverse Transcriptase Polymerase Chain ReactionNF-kappa BProteinsGeneral MedicineIAPCell cycleapoptosiMolecular biologyDrug Resistance MultipleXIAPGene Expression Regulation Neoplasticmedicine.anatomical_structureOncologyDrug Resistance NeoplasmApoptosisCancer researchNAIPmedicine.drugOncology Reports
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Glucose metabolism of malignant cells is not regulated by transketolase-like (TKTL)-1.

2010

An isoenzyme of transketolase, transketolase-like (TKTL)-1, has been hypothesized to play a pivotal role in the pathophysiology of malignant tumors. Available data are based on the detection of the putative TKTL-1 protein with one particular mouse monoclonal anti-TKTL-1 antibody, clone JFC12T10. In this study it was demonstrated that a) JFC12T10 detects multiple unspecific bands in Western blots, b) a 75-kDa band hitherto referred to as TKTL-1 corresponds to a nuclear protein and c) immunohistochemical detection of TKTL-1 in benign leiomyomas yields an expression pattern identical to that found in a variety of malignant tumors. In RT-PCR assays, using three different primer pairs for transk…

Cancer ResearchBlotting WesternClone (cell biology)TransketolaseBiologyIsozymeGene Expression Regulation EnzymologicMiceCell Line TumorNeoplasmsAnimalsHumansNuclear proteinTumor hypoxiaOncogeneLeiomyomaAntibodies MonoclonalCell cycleGene Expression Regulation NeoplasticGlucoseOncologyBiochemistryMonoclonalUterine NeoplasmsCancer researchFemaleTransketolaseHeLa CellsInternational journal of oncology
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Suppression of Mcl-1 via RNA interference sensitizes human hepatocellular carcinoma cells towards apoptosis induction

2006

Abstract Background Hepatocelluar carcinoma (HCC) is one of the most common cancers worldwide and a major cause of cancer-related mortality. HCC is highly resistant to currently available chemotherapeutic drugs. Defects in apoptosis signaling contribute to this resistance. Myeloid cell leukemia-1 (Mcl-1) is an anti-apoptotic member of the Bcl-2 protein family which interferes with mitochondrial activation. In a previous study we have shown that Mcl-1 is highly expressed in tissues of human HCC. In this study, we manipulated expression of the Mcl-1 protein in HCC cells by RNA interference and analyzed its impact on apoptosis sensitivity of HCC cells in vitro. Methods RNA interference was per…

Cancer ResearchCarcinoma HepatocellularMyeloidCellAntineoplastic AgentsApoptosisBiologylcsh:RC254-282RNA interferenceCell Line Tumorhemic and lymphatic diseasesGeneticsmedicineHumansneoplasmsLiver Neoplasmslcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseasedigestive system diseasesIn vitroNeoplasm ProteinsGene Expression Regulation NeoplasticLeukemiamedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2OncologyApoptosisHepatocellular carcinomaCancer researchMyeloid Cell Leukemia Sequence 1 ProteinRNA InterferenceStem cellResearch ArticleBMC Cancer
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Tumor Hypoxia: Causative Factors, Compensatory Mechanisms, and Cellular Response

2004

Abstract Learning Objectives After completing this course, the reader will be able to: Explain the effect of hypoxia on resistance to treatment. Describe the causes of tumor hypoxia. Characterize cellular response to hypoxia. Access and take the CME test online and receive 1 hour of AMA PRA category 1 credit at CME.TheOncologist.com Hypoxia is a characteristic feature of locally advanced solid tumors resulting from an imbalance between oxygen (O2) supply and consumption. Major causative factors of tumor hypoxia are abnormal structure and function of the microvessels supplying the tumor, increased diffusion distances between the nutritive blood vessels and the tumor cells, and reduced O2 tra…

Cancer ResearchCell SurvivalAnemiamedicine.medical_treatmentPhotodynamic therapyDiseaseNeoplasmsmedicineHumansNeovascularization PathologicTumor hypoxiabusiness.industryAnemiaTumor OxygenationHypoxia (medical)medicine.diseaseAdaptation PhysiologicalCell HypoxiaOxygenRadiation therapyCell Transformation NeoplasticOncologyDrug Resistance NeoplasmImmunologyDisease ProgressionCancer researchHemoglobinmedicine.symptombusinessThe Oncologist
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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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Mitochondrial chaperones in cancer: From molecular biology to clinical diagnostics

2006

Mitochondria are cell organelles involved in processes of cell life and death, and therefore also in tumoral transformation. Indeed, mitochondria dysfunction is a prominent feature of cancer cells. Mitochondrial proteins and DNA have also been previously studied as markers of tumorigenesis. Heat shock proteins (HSPs) are ubiquitous evolutionary conserved proteins. HSPs enhance their expression in stressed cells and they are involved in gene expression regulation, DNA replication, signal transduction, differentiation, apoptosis, cellular senescence or immortalization. This review reflects recent views on the role of some mitochondrial molecular chaperones as prohibitin, mortalin and HSP60/HS…

Cancer ResearchCellBiologyMitochondrionmedicine.disease_causeMitochondrial ProteinsNeoplasmsHeat shock proteinmedicineHumanscancerProhibitinHeat-Shock ProteinsPharmacologyMolecular biologyMitochondriaCell biologyCell Transformation Neoplasticmedicine.anatomical_structureOncologyCancer cellMolecular MedicineHSP60Signal transductionCarcinogenesisMolecular ChaperonesCancer Biology & Therapy
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Osteosarcoma cell-derived exosomes affect tumor microenvironment by specific packaging of microRNAs

2018

Abstract Bone microenvironment provides growth and survival signals essential for osteosarcoma (OS) initiation and progression. OS cells regulate communications inside tumor microenvironment through different ways and, among all, tumor-derived exosomes support cancer progression and metastasis. To define the contribution of OS-derived exosomes inside the microenvironment, we investigated the effects induced in bone remodeling mechanism and tumor angiogenesis. We demonstrated that exosomes promoted osteoclasts differentiation and bone resorption activity. Furthermore, exosomes potentiated tube formation of endothelial cells and increased angiogenic markers expression. We therefore investigat…

Cancer ResearchCellBone NeoplasmsBiologyExosomesmedicine.disease_causeCell MovementSettore BIO/13 - Biologia ApplicataosteosarcomamicroRNABiomarkers TumormedicineHumansexosometumor microenvironmentTelomerase reverse transcriptaseCells CulturedCell ProliferationTube formationTumor microenvironmentNeovascularization PathologicGene Expression ProfilingGeneral Medicinemedicine.diseaseMicrovesiclesGene Expression Regulation NeoplasticMicroRNAsmedicine.anatomical_structureCancer researchmicroRNAs profilingOsteosarcomaEndothelium VascularCarcinogenesis
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Whole-epigenome analysis in multiple myeloma reveals DNA hypermethylation of B cell-specific enhancers

2015

Abstract Analyzing the DNA methylome of multiple myeloma (MM), a plasma cell neoplasm, by whole-genome bisulfite sequencing and high-density arrays, we observed regional DNA hypermethylation embedded in extensive global hypomethylation. In contrast to the widely reported DNA hypermethylation of promoter-associated CpG islands (CGIs) in cancer, hypermethylated sites in MM as compared to normal plasma cells were located outside CpG islands and were unexpectedly associated with intronic enhancer regions active in normal B cells. Both RNA-seq and in vitro reporter assays indicated that enhancer hypermethylation is globally associated with downregulation of its host genes. ChIP-seq and DNAseI-se…

Cancer ResearchCellular differentiationCèl·lules BADNBisulfite sequencingImmunologyPlasma CellsDown-RegulationBiologyBiochemistryEpigenesis GeneticEpigènesiCell Line TumorGeneticsMielomatosiHumansEpigeneticsEnhancerPromoter Regions GeneticGeneMolecular BiologyGenetics (clinical)EpigenomicsB cellsGenome HumanResearchCell DifferentiationMethylationDNACell BiologyHematologyDNA NeoplasmPlasma cell neoplasmDNA MethylationMolecular biologyMyeloproliferative disordersGene Expression Regulation NeoplasticEnhancer Elements GeneticOncologyCpG siteDNA methylationNeoplastic Stem CellsCpG IslandsMultiple MyelomaEpigenesisTranscription FactorsGenome Research
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