Search results for "Neoplastic"

showing 10 items of 2901 documents

Mitochondrial localization and temporal expression of the Drosophila melanogaster DnaJ homologous tumor suppressor Tid50

1998

The Drosophila melanogaster tumor suppressor gene lethal(2)tumorous imaginal discs (tid) was identified as a homolog of all dnaJ-like genes known to date which have been well preserved in evolution. Homozygous D. melanogaster l(2)tid mutants l(2)tid1, l(2)tid2 and l(2)tid3 are characterized by neoplastic transformation of the adult integumental primordia, the imaginal discs, and the death at the time of puparium formation. The first part of this study is concerned with the identification and subcellular localization of the l(2)tid-encoded protein, Tid50. The second part examines its tissue specific expression during wild-type development and in tumorous imaginal discs. To specify the functi…

Embryo NonmammalianTumor suppressor geneMutantGenes InsectCell FractionationBiochemistryCell LineMitochondrial ProteinsMelanogasterAnimalsDrosophila ProteinsGenes Tumor SuppressorNeoplastic transformationRNA MessengerGeneHeat-Shock ProteinsbiologyPupaGene Expression Regulation DevelopmentalRNANeoplasms ExperimentalSequence Analysis DNAOriginal ArticlesCell BiologyHSP40 Heat-Shock Proteinsbiology.organism_classificationMolecular biologyMitochondriaGene Expression Regulation NeoplasticImaginal discDrosophila melanogasterOrgan SpecificityLarvaRabbitsDrosophila melanogasterCell Stress & Chaperones
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Overexpression of the truncated form of high mobility group a proteins (HMGA2) in human myometrial cells induces leiomyoma-like tissue formation

2014

The pathogenesis of uterine leiomyomas, the most common benign tumor in women, is still unknown. This lack of basic knowledge limits the development of novel non-invasive therapies. Our group has previously demonstrated that leiomyoma side population (SP) cells are present in tumor lesions and act like putative tumor-initiating stemcells in human leiomyoma. Moreover, accumulated evidence demonstrates that these benign tumors of mesenchymal origin are characterized by rearrangements of the High Mobility Group A proteins (HMGA). In this work, we tested the hypothesis that leiomyoma development may be due to overexpression of HMGA2 (encoding high mobility group AT-hook2) in myometrial stem cel…

EmbryologyMice SCID//purl.org/becyt/ford/1 [https]MiceMice Inbred NODProtein IsoformsUterine leiomyomaLeiomyomaStem CellsSOMATIC STEM CELLSObstetrics and GynecologyExonsBioquímica y Biología Molecularfemale genital diseases and pregnancy complicationsGene Expression Regulation NeoplasticCell Transformation NeoplasticLeiomyomaUterine NeoplasmsMyometriumNeoplastic Stem CellsFemaleStem cellHIGH MOBILITY GROUP A PROTEINSCIENCIAS NATURALES Y EXACTASPlasmidsAdult stem cellmedicine.medical_specialtyUTERINE LEIOMYOMASMyocytes Smooth MuscleTransplantation HeterologousBiologyTransfectionHUMAN MYOMETRIUMCiencias BiológicasHMGA2Side populationInternal medicineGeneticsmedicineAnimalsHumans//purl.org/becyt/ford/1.6 [https]neoplasmsMolecular BiologyHMGA2 ProteinMesenchymal stem cellHMGASIDE POPULATIONCell Biologymedicine.diseaseIntronsEndocrinologyReproductive MedicineCancer researchbiology.proteinDevelopmental Biology
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Cloning of Several Genes Coding for Retinoic Acid Nuclear Receptors in the Mouse Embryonal Carcinoma Cell Line PCC7–MZ1

1993

Mouse embryonal carcinoma cell line PCC7-Mz1 can be induced by retinoic acid (RA) to differentiate into several well defined phenotypes of neuroectodermal origin (Lang, E. et al. (1989) J. Cell. Biol. 109, 2481-2493). Several subclones of the cell line (clonal variants) differ from each other in their developmental potential. To test whether these differences in cellular fate are due to somatic mutations in specific genes of these cells, we have cloned full length cDNAs coding for the alpha 1 and beta 2 isoforms, and partial length cDNAs coding for the alpha 2, beta 1 and beta 3 isoforms of the retinoic acid nuclear receptor (RAR). The cloned cDNAs did not differ in sequence from those of n…

Embryonal Carcinoma Stem CellsReceptors Retinoic AcidSomatic cellCellular differentiationMolecular Sequence DataRetinoic acidTretinoinBiologyEmbryonal carcinomaMicechemistry.chemical_compoundTumor Cells CulturedmedicineAnimalsHumansAmino Acid SequenceCloning MolecularPromoter Regions GeneticGenePharmacologyCloningBase SequenceNuclear ProteinsEmbryonal Carcinoma Stem CellsCell DifferentiationDNAmedicine.diseaseMolecular biologyRecombinant ProteinsRetinoic acid receptorchemistryNeoplastic Stem CellsCarrier ProteinsJournal of Receptor Research
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Adverse events associated with encorafenib plus binimetinib in the COLUMBUS study: incidence, course and management.

2019

Abstract Background Dual inhibition of the mitogen-activated protein kinase pathway with BRAF/MEK inhibitor (BRAFi/MEKi) therapy is a standard treatment for BRAFV600-mutant metastatic melanoma and has historically been associated with grade III pyrexia or photosensitivity depending on the combination used. The objective of this study was to fully describe adverse events from the COLUMBUS study evaluating the most recent BRAF/MEK inhibitor combination encorafenib+binimetinib. Patients and methods Patients with locally advanced, unresectable or metastatic BRAFV600-mutant melanoma were randomised to receive encorafenib 450 mg once daily plus binimetinib 45 mg twice daily, encorafenib 300 mg on…

Encorafenib0301 basic medicineOncologyMaleCancer ResearchSkin NeoplasmsBinimetinib; Encorafenib; Melanoma; Safety; Vemurafenib;MedizinBinimetinibchemistry.chemical_compound0302 clinical medicineAntineoplastic Combined Chemotherapy Protocols1306 Cancer ResearchVemurafenibMelanomaFatigueeducation.field_of_studySulfonamidesMEK inhibitorMelanomaStandard treatmentIncidence10177 Dermatology ClinicBinimetinibNauseaMiddle AgedOncology030220 oncology & carcinogenesis2730 OncologyFemaleSafetyMitogen-Activated Protein Kinasesmedicine.drugProto-Oncogene Proteins B-rafmedicine.medical_specialtyVomitingPopulation610 Medicine & health03 medical and health sciencesInternal medicinemedicineHumanseducationAdverse effectProtein Kinase Inhibitorsbusiness.industrymedicine.diseaseDiscontinuation030104 developmental biologychemistryVemurafenibMutationBenzimidazolesCarbamatesbusinessEuropean journal of cancer (Oxford, England : 1990)
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Preventive effect of risedronate on bone loss and frailty fractures in elderly women treated with anastrozole for early breast cancer.

2011

The aim of this study was to assess the effect of adjuvant anastrozole, alone or associated with risedronate, on BMD and bone fracture risk in women more than 70 years old with hormone receptor-positive early breast cancer (EBC). In a group of 51 elderly women (aged 76.4 ± 5.0 years) considered for adjuvant aromatase inhibitors for EBC, 24 patients with T-scores ≥ -2 and no prevalent fractures received anastrozole 1 mg/day (group A), and 27 patients with T-scores < -2, or with T-scores ≥ -2 and prevalent fractures (group B), received anastrozole (1 mg/day) plus risedronate (35 mg/week). Both groups received supplementation with 1 g calcium carbonate and 800 IU vitamin D per day. Differen…

Endocrinology Diabetes and MetabolismOsteoporosisSeverity of Illness IndexCohort StudiesEndocrinologyBone DensityOrthopedics and Sports MedicineVitamin DAromataseOsteoporosis PostmenopausalAged 80 and overBone Density Conservation AgentsbiologyAromatase InhibitorsEtidronic AcidGeneral MedicineCombined Modality Therapymedicine.anatomical_structureFemaleRisedronic Acidmedicine.drugmusculoskeletal diseasesmedicine.medical_specialtyAntineoplastic Agents HormonalUrologyAnastrozoleBreast NeoplasmsAnastrozoleCalcium CarbonateNitrilesmedicineVitamin D and neurologyHumansBone ResorptionAgedNeoplasm StagingFemoral neckTrochanterbusiness.industryBone fractureTriazolesmedicine.diseaseSurgeryEarly breast cancer Anastrozole Osteoporosis Vertebral fractures ElderlyDietary SupplementsOrthopedic surgerybiology.proteinbusinessOsteoporotic FracturesFollow-Up Studies
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Unjamming overcomes kinetic and proliferation arrest in terminally differentiated cells and promotes collective motility of carcinoma.

2019

During wound repair, branching morphogenesis and carcinoma dissemination, cellular rearrangements are fostered by a solid-to-liquid transition, known as unjamming. The biomolecular machinery behind unjamming and its pathophysiological relevance remain, however, unclear. Here, we study unjamming in a variety of normal and tumorigenic epithelial two-dimensional (2D) and 3D collectives. Biologically, the increased level of the small GTPase RAB5A sparks unjamming by promoting non-clathrin-dependent internalization of epidermal growth factor receptor that leads to hyperactivation of the kinase ERK1/2 and phosphorylation of the actin nucleator WAVE2. This cascade triggers collective motility effe…

EndosomeCellular differentiationmedia_common.quotation_subjectMotility02 engineering and technologySettore MED/08 - Anatomia Patologica010402 general chemistry01 natural sciencesExtracellular matrixCell MovementCell Line TumorHumansGeneral Materials ScienceSmall GTPaseEpidermal growth factor receptorInternalizationActinmedia_commonCell Proliferationrab5 GTP-Binding ProteinsMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3biologyChemistryMechanical EngineeringCell DifferentiationGeneral Chemistry021001 nanoscience & nanotechnologyCondensed Matter Physics0104 chemical sciencesCell biologyErbB ReceptorsKineticscarcinoma differentiated neoplastic cellsMechanics of Materialsbiology.protein0210 nano-technologyNature materials
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Positioning Europe for the EPITRANSCRIPTOMICS challenge

2018

WOS: 000444092300018 PubMed ID: 29671387 The genetic alphabet consists of the four letters: C, A, G, and T in DNA and C,A,G, and U in RNA. Triplets of these four letters jointly encode 20 different amino acids out of which proteins of all organisms are built. This system is universal and is found in all kingdoms of life. However, bases in DNA and RNA can be chemically modified. In DNA, around 10 different modifications are known, and those have been studied intensively over the past 20years. Scientific studies on DNA modifications and proteins that recognize them gave rise to the large field of epigenetic and epigenomic research. The outcome of this intense research field is the discovery t…

Epigenomics0301 basic medicine[SDV]Life Sciences [q-bio]Gene ExpressionDetection of RNA ModificationEpigenesis GeneticTranscriptomechemistry.chemical_compoundEcologyEvolution & EthologyNeoplasmsRNA NeoplasmEuropean FundingComputingMilieux_MISCELLANEOUSRNA Neoplasm/geneticsEpitranscriptomicsEpigenomicsStem CellsDNA NeoplasmNeoplasms/genetics[SDV] Life Sciences [q-bio]EuropeGene Expression Regulation NeoplasticDetection of RNA modificationGenetics & GenomicsComputational biologyBiologyBiochemistry & ProteomicsENCODE03 medical and health sciencesEpigenomics/standardsEpitranscriptomicsModel systemsHumansEpigeneticsDatabase of ModificationDNA Neoplasm/geneticsMolecular BiologyComputational & Systems BiologyEuropean funding[SDV.GEN]Life Sciences [q-bio]/GeneticsGene Expression ProfilingFOS: Clinical medicineNeurosciencesModel SystemsRNACell Biology030104 developmental biologychemistryGene Expression Profiling/methodsAlphabetTranscriptomeDNARNA Biology
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Genome-wide promoter methylation analysis in neuroblastoma identifies prognostic methylation biomarkers.

2012

Background: Accurate outcome prediction in neuroblastoma, which is necessary to enable the optimal choice of risk-related therapy, remains a challenge. To improve neuroblastoma patient stratification, this study aimed to identify prognostic tumor DNA methylation biomarkers.Results: To identify genes silenced by promoter methylation, we first applied two independent genome-wide methylation screening methodologies to eight neuroblastoma cell lines. Specifically, we used re-expression profiling upon 5-aza-2'-deoxycytidine (DAC) treatment and massively parallel sequencing after capturing with a methyl-CpG-binding domain (MBD-seq). Putative methylation markers were selected from DAC-upregulated …

EpigenomicsMYCN Single CopyMedizinPrimary Neuroblastoma TumorBioinformaticsNeuroblastoma0302 clinical medicineRisk FactorsMYCN StatusDatabases GeneticPromoter MethylationGTP-Binding Protein alpha Subunits GsHazard Ratio PatientPromoter Regions GeneticEpigenomicsRegulation of gene expression0303 health sciencesMassive parallel sequencingHigh-Throughput Nucleotide SequencingMethylation3. Good healthGene Expression Regulation NeoplasticMedizinische Fakultät » Universitätsklinikum Essen » Zentrum für Kinder- und Jugendmedizin030220 oncology & carcinogenesisDNA methylationAzacitidineBiologieBiologyDecitabine03 medical and health sciencesneuroblastomaCell Line TumorNeuroblastomaBiomarkers TumorChromograninsmedicineHumansddc:61ddc:610Epigenetics030304 developmental biologyepigeneticsGenome HumanResearchBiology and Life SciencesbiomarkersSequence Analysis DNADNA MethylationHCT116 Cellsmedicine.diseaseSurvival AnalysisCancer researchHuman genomeDNA-methylation
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Network pharmacology of cancer: From understanding of complex interactomes to the design of multi-target specific therapeutics from nature

2015

Despite massive investments in drug research and development, the significant decline in the number of new drugs approved or translated to clinical use raises the question, whether single targeted drug discovery is the right approach. To combat complex systemic diseases that harbour robust biological networks such as cancer, single target intervention is proved to be ineffective. In such cases, network pharmacology approaches are highly useful, because they differ from conventional drug discovery by addressing the ability of drugs to target numerous proteins or networks involved in a disease. Pleiotropic natural products are one of the promising strategies due to their multi-targeting and d…

EpigenomicsProteomics0301 basic medicineDrugmedia_common.quotation_subjectSystems biologyGene regulatory networkSynthetic lethalityDiseaseComputational biologyBiologyPharmacology03 medical and health sciencesNeoplasmsDrug DiscoveryBiomarkers TumormedicineAnimalsHumansMetabolomicsGene Regulatory NetworksMolecular Targeted TherapyProtein Interaction Mapsmedia_commonPharmacologyPlants MedicinalDrug discoveryGene Expression ProfilingSystems BiologyCancermedicine.diseaseAntineoplastic Agents PhytogenicGene Expression Regulation Neoplastic030104 developmental biologyBiological networkPhytotherapySignal TransductionPharmacological Research
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Dysplasia in oral lichen planus: relevance, controversies and challenges. A position paper

2021

Background: Patients with oral lichen planus (OLP) have an increased risk of oral cancer. For this reason, OLP is classified as an oral potentially malignant disorder. However, the precise personal (or individual) risk is unknown. Recent meta-analytical studies have reported that dysplastic OLP may transform to cancer in around 6% of cases, while the rate of transformation is lower (<1.5%) in non-dysplastic cases. The presence of epithelial dysplasia has emerged as the most powerful indicator for assessing cancer risk in oral potentially malignant disorders in routine practice. However, the general acceptance of epithelial dysplasia as an accompanying histologic feature in OLP is subject to…

Epithelial dysplasiamedicine.medical_specialtyBiopsyReviewEpithelial dysplasiaMalignancytastestomatognathic systemOral Cancer and Potentially malignant disordersBiopsyOral and maxillofacial pathologymedicineHumansGeneral DentistryUNESCO:CIENCIAS MÉDICASMouth neoplasmchildHyperplasiamedicine.diagnostic_testoral mucosabusiness.industryOral cancerCancermedicine.diseaseDermatologystomatognathic diseasesCell Transformation NeoplasticOtorhinolaryngologycovid-19DysplasiaOral lichen planusSurgeryOral lichen planusMouth NeoplasmsbusinessMouth DiseasesLichen Planus Oral
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