Search results for " Neoplastic"

showing 10 items of 662 documents

Novel circulating microRNA signature as a potential non-invasive multi-marker test in ER-positive early-stage breast cancer:A case control study

2014

Introduction There are currently no highly sensitive and specific minimally invasive biomarkers for detection of early‐stage breast cancer. MicroRNAs (miRNAs) are present in the circulation and may be unique biomarkers for early diagnosis of human cancers. The aim of this study was to investigate the differential expression of miRNAs in the serum of breast cancer patients and healthy controls. Methods Global miRNA analysis was performed on serum from 48 patients with ER‐positive early‐stage breast cancer obtained at diagnosis (24 lymph node‐positive and 24 lymph node‐negative) and 24 age‐matched healthy controls using LNA‐based quantitative real‐time PCR (qRT‐PCR). A signature of miRNAs was…

Genetic MarkersOncologyCancer Researchmedicine.medical_specialtyEstrogen receptorBreast NeoplasmsBiologyReal-Time Polymerase Chain ReactionBioinformaticsSerum markersBreast cancerBreast cancerInternal medicinemicroRNABiomarkers TumorGeneticsmedicineHumansBreastStage (cooking)Lymph nodeResearch ArticlesAgedmiRNAReceiver operating characteristicGene Expression ProfilingCase-control studyGeneral MedicineMiddle Agedmedicine.diseaseGene Expression Regulation NeoplasticMicroRNAsCirculating MicroRNAmedicine.anatomical_structureReceptors EstrogenOncologyCase-Control StudiesMolecular MedicineFemaleMiRNAResearch Article
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Liver-specific overexpression of matrix metalloproteinase 9 (MMP-9) in transgenic mice accelerates development of hepatocellular carcinoma.

2010

Matrix metalloproteinase-9 (MMP-9) plays a central role in tumor invasion and development of metastases. Expression of MMP-9 had been shown in human hepatocellular carcinomas (HCCs). However, it remained unclear whether MMP-9 could influence development of HCC. In order to address this issue, we generated transgenic mice overexpressing MMP-9 in the liver. In order to avoid embryonic lethality a Cre-lox system was utilized for conditional overexpression of MMP-9 under control of an albumin enhancer and promoter. Induction of MMP-9 overexpression in transgenic mice was achieved by i.v. injection of an adenovirus coding for the Cre recombinase. Initiation of liver carcinogenesis was achieved b…

Genetically modified mouseCancer ResearchLiver tumorTransgeneGenetic VectorsCre recombinaseGene ExpressionMice TransgenicBiologymedicine.disease_causeMiceLiver Neoplasms ExperimentalIn vivoGene OrdermedicineAnimalsHomeostasisHumansHomologous RecombinationMolecular BiologyIntegrasesHCCSmedicine.diseaseMolecular biologyCell Transformation NeoplasticPhenotypeLiverMatrix Metalloproteinase 9Organ SpecificityHepatocellular carcinomaCarcinogenesisMolecular carcinogenesis
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Inhibition of the HER2 pathway by n-3 polyunsaturated fatty acids prevents breast cancer in fat-1 transgenic mice

2013

Overexpression of the tyrosine kinase receptor, ErbB2/HER2/Neu, occurs in 25–30% of invasive breast cancer (BC) with poor patient prognosis. Due to confounding factors, inconsistencies still remain regarding the protective effects of n-3 polyunsaturated fatty acids (PUFAs) on BC. We therefore evaluated whether fat-1 transgenic mice, endogenously synthesizing n-3 PUFAs from n-6 PUFAs, were protected against BC development, and we then aimed to study in vivo a mechanism potentially involved in such protection. E0771 BC cells were implanted into fat-1 and wild-type (WT) mice. After tumorigenesis examination, we analyzed the expression of proteins involved in the HER2 signaling pathway and lipi…

Genetically modified mouseFatty Acid DesaturasesDocosahexaenoic AcidsReceptor ErbB-3Receptor ErbB-2Breast NeoplasmsMice TransgenicQD415-436Biologymedicine.disease_causexenograft preventionBiochemistryReceptor tyrosine kinaseProto-Oncogene Proteins c-mycMiceEndocrinologyDownregulation and upregulationCell Line TumorFatty Acids Omega-3medicineAnimalsHumansCaenorhabditis elegans ProteinsResearch ArticlesCell Proliferationchemistry.chemical_classificationCell growthCell BiologyXenograft Model Antitumor AssaysGene Expression Regulation NeoplasticMice Inbred C57BLchemistryDocosahexaenoic acidImmunologyn-3 tissue enrichmentbiology.proteinCancer researchFemaleSignal transductionCarcinogenesispolyunsaturated fatty acid-derived mediatorsPolyunsaturated fatty acidSignal TransductionJournal of Lipid Research
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Role of the insulin-like growth factor system in adrenocortical growth control and carcinogenesis.

2004

Clinically silent adrenocortical adenomas are the most frequent abnormalities in the adrenal gland. In contrast, adrenocortical carcinoma is a rare tumor with an extremely poor prognosis. The factors responsible for the frequent occurrence of benign adrenocortical tumors on one hand and the rare malignant transformation on the other are not known. Several genetic alterations such as loss of imprinting or loss of heterozygosity of the 11p15 gene locus causing a strong IGF-II overexpression have been demonstrated in the majority of adrenocortical carcinomas. In addition to IGF-II overexpression, increased levels of the IGF-I-receptor and IGFBP-2 have been found in advanced human adrenocortica…

Genetically modified mousemedicine.medical_specialtyEndocrinology Diabetes and Metabolismmedicine.medical_treatmentClinical BiochemistryAdrenal Gland NeoplasmsLoss of HeterozygosityBiologymedicine.disease_causeBiochemistryMalignant transformationReceptor IGF Type 1Loss of heterozygosityInsulin-like growth factorMiceEndocrinologyInsulin-Like Growth Factor IIInternal medicineCell Line TumormedicineAdrenocortical carcinomaAnimalsHumansNeoplastic transformationNeoplastic ProcessesAdrenal glandChromosomes Human Pair 11Biochemistry (medical)CarcinomaGeneral Medicinemedicine.diseaseGene Expression Regulation NeoplasticInsulin-Like Growth Factor Binding Protein 2medicine.anatomical_structureEndocrinologyCarcinogenesisSignal TransductionHormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme
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A BMP7 Variant Inhibits Tumor Angiogenesis In Vitro and In Vivo through Direct Modulation of Endothelial Cell Biology

2015

Bone morphogenetic proteins (BMPs), members of the TGF-β superfamily, have numerous biological activities including control of growth, differentiation, and vascular development. Using an in vitro co-culture endothelial cord formation assay, we investigated the role of a BMP7 variant (BMP7v) in VEGF, bFGF, and tumor-driven angiogenesis. BMP7v treatment led to disruption of neo-endothelial cord formation and regression of existing VEGF and bFGF cords in vitro. Using a series of tumor cell models capable of driving angiogenesis in vitro, BMP7v treatment completely blocked cord formation. Pre-treatment of endothelial cells with BMP7v significantly reduced their cord forming ability, indicating …

Genetics and Molecular Biology (all)MaleVascular Endothelial Growth Factor AFibroblast Growth FactorAngiogenesisBone Morphogenetic Protein 7Nudelcsh:MedicineSmad ProteinsFibroblast growth factorBiochemistryNeovascularizationMiceCell Movementlcsh:ScienceBMP7 Angiogenesis TumorTumorMultidisciplinaryCell DeathNeovascularization PathologicMedicine (all)Cell migrationCell biologyEndothelial stem cellSettore MED/26 - NEUROLOGIAVascular endothelial growth factor ADrug CombinationsAdipose TissueAdipose Tissue; Animals; Bone Morphogenetic Protein 7; Cell Death; Cell Line Tumor; Cell Movement; Cell Proliferation; Collagen; Drug Combinations; Endothelial Cells; Fibroblast Growth Factor 2; Glioblastoma; Human Umbilical Vein Endothelial Cells; Humans; Laminin; Male; Mice Nude; Neoplastic Stem Cells; Neovascularization Pathologic; Neovascularization Physiologic; Proteoglycans; Receptor Fibroblast Growth Factor Type 1; Signal Transduction; Smad Proteins; Vascular Endothelial Growth Factor A; Vascular Endothelial Growth Factor Receptor-2; Xenograft Model Antitumor Assays; Biochemistry Genetics and Molecular Biology (all); Agricultural and Biological Sciences (all)Neoplastic Stem CellsFibroblast Growth Factor 2ProteoglycansCollagenmedicine.symptomReceptorType 1Research ArticleSignal TransductionMice NudeNeovascularization PhysiologicBMP7BiologyCell LineSettore MED/04 - PATOLOGIA GENERALECell Line TumormedicineHuman Umbilical Vein Endothelial CellsAnimalsHumansAgricultural and Biological Sciences (all); Biochemistry Genetics and Molecular Biology (all); Medicine (all)Receptor Fibroblast Growth Factor Type 1PhysiologicNeovascularizationCell ProliferationPathologicMatrigelBiochemistry Genetics and Molecular Biology (all)lcsh:REndothelial CellsKinase insert domain receptorVascular Endothelial Growth Factor Receptor-2Xenograft Model Antitumor AssaysAgricultural and Biological Sciences (all)lcsh:QAngiogenesisLamininGlioblastomaPLoS ONE
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Mitochondrial DNA mutations in cancer--from bench to bedside.

2009

Mitochondria are cell organelles mostly known for their production of ATP through oxidative phosphorylation. As suggested over 70 years ago by O. Warburg and recently confirmed with molecular techniques, alterations in respiratory activity and mitochondrial DNA appear to be a common feature of malignant cells. Somatic mtDNA mutations have been reported in many types of cancer cells. MtDNA mutation pattern may enhance the specificity of cancer diagnostics, detection and prediction of tumor growth rate and patients' outcome. Therefore it may be used as a molecular cancer bio-marker. Nevertheless recently published papers list a large number of mitochondrial DNA mutations in many different can…

GeneticsMutationMitochondrial DNASettore BIO/16 - Anatomia UmanaSomatic cellRespiratory chainCancerContext (language use)ApoptosisMitochondrionBiologymedicine.disease_causemedicine.diseaseDNA MitochondrialModels BiologicalTranslational Research BiomedicalCell Transformation NeoplasticNeoplasmsCancer cellMutationmedicineHumansCancer Mitochondria Molecular Marker Mutation OXPHOS ReviewReactive Oxygen SpeciesCell ProliferationFrontiers in bioscience (Landmark edition)
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Genetics of hepatocellular carcinoma.

2007

The completely assembled human genome has made it possible for modern medicine to step into an era rich in genetic information and high-throughput genomic analysis. These novel and readily available genetic resources and analytical tools may be the key to unravel the molecular basis of hepatocellular carcinoma (HCC). Moreover, since an efficient treatment for this disease is lacking, further understanding of the genetic background of HCC will be crucial in order to develop new therapies aimed at selected targets. We report on the current status and recent developments in HCC genetics. Special emphasis is given to the genetics and regulation of major signalling pathways involved in HCC such …

GeneticsRegulation of gene expressionChromosome AberrationsModern medicineMutationCarcinoma HepatocellularMicroarray analysis techniquesLiver NeoplasmsGastroenterologyGenomicsGeneral MedicineDNA NeoplasmBiologyDNA Methylationmedicine.disease_causedigestive system diseasesGene expression profilingGene Expression Regulation NeoplasticEditorialDNA methylationmedicineHumansHuman genomeOligonucleotide Array Sequence AnalysisSignal TransductionWorld journal of gastroenterology
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Hypoxia and anemia: effects on tumor biology and treatment resistance

2004

In locally advanced solid tumors, oxygen (O2) delivery is frequently reduced or even abolished. This is due to abnormalities of the tumor microvasculature, adverse diffusion geometries, and tumor-associated and/or therapy-induced anemia. Up to 50-60% of locally advanced solid tumors may exhibit hypoxic and/or anoxic tissue areas that are heterogeneously distributed within the tumor mass. In approximately 30% of pretreatment patients, a decreased O2 transport capacity of the blood as a result of tumor-associated anemia can greatly contribute to the development of tumor hypoxia. While normal tissues can compensate for this O2 deficiency status by a rise in blood flow rate, locally advanced tu…

Genome instabilityAnemiaClinical BiochemistryDrug resistanceBiologyRadiation ToleranceNeoplasmsmedicineHumansHypoxiaRegulation of gene expressionTumor hypoxiaBiochemistry (medical)NF-kappa BNuclear ProteinsAnemiaHematologyHypoxia (medical)Hypoxia-Inducible Factor 1 alpha SubunitPrognosismedicine.diseaseNeoplasm ProteinsDNA-Binding ProteinsGene Expression Regulation NeoplasticOxygenHypoxia-inducible factorsDrug Resistance NeoplasmTumor progressionImmunologyDisease ProgressionCancer researchHypoxia-Inducible Factor 1medicine.symptomCell DivisionTranscription FactorsTransfusion Clinique et Biologique
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Simultaneous Aurora-A/STK15 overexpression and centrosome amplification induce chromosomal instability in tumour cells with a MIN phenotype

2007

Abstract Background Genetic instability is a hallmark of tumours and preneoplastic lesions. The predominant form of genome instability in human cancer is chromosome instability (CIN). CIN is characterized by chromosomal aberrations, gains or losses of whole chromosomes (aneuploidy), and it is often associated with centrosome amplification. Centrosomes control cell division by forming a bipolar mitotic spindle and play an essential role in the maintenance of chromosomal stability. However, whether centrosome amplification could directly cause aneuploidy is not fully established. Also, alterations in genes required for mitotic progression could be involved in CIN. A major candidate is represe…

Genome instabilityCancer ResearchCellular differentiationAneuploidyApoptosisCell CommunicationSpindle ApparatusBiologyProtein Serine-Threonine Kinaseslcsh:RC254-282Aurora KinasesChromosome instabilityChromosomal InstabilitymedicineTumor Cells CulturedGeneticsHumansRNA Small InterferingMitosisIn Situ Hybridization FluorescenceAurora Kinase ACentrosomePloidiesReverse Transcriptase Polymerase Chain ReactionAurora-A centrosomes amplification aneuploidyCell Differentiationlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseAneuploidyCell biologySpindle apparatusUp-RegulationSettore BIO/18 - GeneticaCell Transformation NeoplasticPhenotypeMicroscopy FluorescenceOncologyCentrosomeColonic NeoplasmsEctopic expressionMicrosatellite InstabilityResearch ArticleBMC Cancer
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Tumor microenvironmental physiology and its implications for radiation oncology.

2004

Abstract The microenvironmental physiology of tumors is uniquely different from that of normal tissues. It is characterized, inter alia, by O 2 depletion (hypoxia, anoxia), glucose and energy deprivation, high lactate levels, and extracellular acidosis, parameters that are anisotropically distributed within the tumor mass. This hostile microenvironment is largely dictated by the abnormal tumor vasculature and heterogeneous microcirculation. Hypoxia and other hostile microenvironmental parameters are known to directly or indirectly confer resistance to irradiation leading to treatment failure. Hypoxia directly leads to a reduced "fixation" of radiation-induced DNA damage. Indirect mechanisms…

Genome instabilityCancer ResearchDNA RepairDNA damagebusiness.industryMicrocirculationPhysiologyHydrogen-Ion ConcentrationCell HypoxiaMicrocirculationGene Expression Regulation NeoplasticOncologyTumor progressionNeoplasmsGene expressionProteomemedicineExtracellularRadiation OncologyHumansRadiology Nuclear Medicine and imagingmedicine.symptombusinessAcidosisSeminars in radiation oncology
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