Search results for " Neoplastic"

showing 10 items of 662 documents

Interrelationship between miRNA and splicing factors in pancreatic ductal adenocarcinoma

2021

Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal cancers because of diagnosis at late stage and inherent/acquired chemoresistance. Recent advances in genomic profiling and biology of this disease have not yet been translated to a relevant improvement in terms of disease management and patient’s survival. However, new possibilities for treatment may emerge from studies on key epigenetic factors. Deregulation of microRNA (miRNA) dependent gene expression and mRNA splicing are epigenetic processes that modulate the protein repertoire at the transcriptional level. These processes affect all aspects of PDAC pathogenesis and have great potential to unravel new therapeutic targets…

0301 basic medicineCancer Researchsplicing deregulationinteractionDiseaseBiologymedicine.disease_causeinteraction; miRNA; PDAC; splicing deregulation; splicing modulation03 medical and health sciencesSplicing factor0302 clinical medicineDownregulation and upregulationCell Line TumormicroRNAGene expressionmedicineHumansEpigeneticsMolecular BiologymiRNAPDACDNA MethylationGene Expression Regulation NeoplasticPancreatic NeoplasmsRepressor ProteinsMicroRNAs030104 developmental biology030220 oncology & carcinogenesisRNA splicingCancer researchKRASRNA Splicing Factorssplicing modulationCarcinoma Pancreatic Ductal
researchProduct

Integrative analysis of key candidate genes and signaling pathways in autoimmune thyroid dysfunction related to anti-CTLA-4 therapy by bioinformatics

2020

Summary Cytotoxic T lymphocyte-associated antigen-4 (CTLA-4), the first immune checkpoint to be targeted clinically, has provided an effective treatment option for various malignancies. However, the clinical advantages associated with CTLA-4 inhibitors can be offset by the potentially severe immune-related adverse events (IRAEs), including autoimmune thyroid dysfunction. To investigate the candidate genes and signaling pathways involving in autoimmune thyroid dysfunction related to anti-CTLA-4 therapy, integrated differentially expressed genes (DEGs) were extracted from the intersection of genes from Gene Expression Omnibus (GEO) datasets and text mining. The functional enrichment was perfo…

0301 basic medicineCandidate geneCD74Signaling pathway.FCGR2BDifferentially expressed geneBiologyBioinformaticsHyperthyroidismAutoimmune Diseases03 medical and health sciencesMice0302 clinical medicineHypothyroidismmedicineAnimalsHumansPharmacology (medical)CTLA-4 AntigenProtein Interaction MapsKEGGGeneImmune Checkpoint InhibitorsPharmacologyPreclinical StudiesSignaling pathwayCancerComputational Biologymedicine.diseaseImmune checkpointGene Expression Regulation Neoplastic030104 developmental biologyGene OntologyAutoimmune thyroid dysfunctionOncologyCTLA-4030220 oncology & carcinogenesisDifferentially expressed genesCTLA-4BiomarkersImmune checkpoint blockadeSignal Transduction
researchProduct

Identification of loci of functional relevance to Barrett's esophagus and esophageal adenocarcinoma: Cross-referencing of expression quantitative tra…

2019

Esophageal adenocarcinoma (EA) and its precancerous condition Barrett's esophagus (BE) are multifactorial diseases with rising prevalence rates in Western populations. A recent meta-analysis of genome-wide association studies (GWAS) data identified 14 BE/EA risk loci located in non-coding genomic regions. Knowledge about the impact of non-coding variation on disease pathology is incomplete and needs further investigation. The aim of the present study was (i) to identify candidate genes of functional relevance to BE/EA at known risk loci and (ii) to find novel risk loci among the suggestively associated variants through the integration of expression quantitative trait loci (eQTL) and genetic…

0301 basic medicineCandidate geneEsophageal MucosaEsophageal NeoplasmsMedizinGene ExpressionGenome-wide association study0302 clinical medicineMathematical and Statistical TechniquesGeneticsMultidisciplinarySodium-Hydrogen Exchanger 3QStatisticsRGenomicsMetaanalysisGene Expression Regulation NeoplasticResearch Design030220 oncology & carcinogenesisPhysical SciencesMedicineResearch Articlemedicine.medical_specialtyScienceQuantitative Trait LociReplication StudiesContext (language use)BiologyAdenocarcinomaResearch and Analysis MethodsPolymorphism Single NucleotideMolecular Genetics03 medical and health sciencesBarrett EsophagusMolecular geneticsmedicineGeneticsGenome-Wide Association StudiesHumansGenetic Predisposition to DiseaseGene RegulationStatistical MethodsGeneMolecular BiologyGenetic associationProteinsBiology and Life SciencesComputational BiologyHuman Geneticsmedicine.diseaseGenome AnalysisRepressor Proteins030104 developmental biologyGenetic LociBarrett's esophagusExpression quantitative trait lociGenetics of DiseaseMathematicsGenome-Wide Association StudyPloS one
researchProduct

c-Fos induces chondrogenic tumor formation in immortalized human mesenchymal progenitor cells

2018

Mesenchymal progenitor cells (MPCs) have been hypothesized as cells of origin for sarcomas, and c-Fos transcription factor has been showed to act as an oncogene in bone tumors. In this study, we show c-Fos is present in most sarcomas with chondral phenotype, while multiple other genes are related to c-Fos expression pattern. To further define the role of c-Fos in sarcomagenesis, we expressed it in primary human MPCs (hMPCs), immortalized hMPCs and transformed murine MPCs (mMPCs). In immortalized hMPCs, c-Fos expression generated morphological changes, reduced mobility capacity and impaired adipogenic- and osteogenic-differentiation potentials. Remarkably, immortalized hMPCs or mMPCs express…

0301 basic medicineCarcinogenesisCelllcsh:MedicineMice SCIDArticleCell Line03 medical and health sciencesMice0302 clinical medicineMice Inbred NODmedicineAnimalsHumansProgenitor celllcsh:ScienceRegulation of gene expressionMultidisciplinaryOncogeneChemistryMesenchymal stem celllcsh:RGenes fosMesenchymal Stem CellsSarcomaChondrogenesisPhenotypeCell biologyGene Expression Regulation Neoplastic030104 developmental biologymedicine.anatomical_structureCell Transformation NeoplasticCell culture030220 oncology & carcinogenesislcsh:QProto-Oncogene Proteins c-fos
researchProduct

Mcl-1 targeting could be an intriguing perspective to cure cancer

2018

The Bcl-2 family, which plays important roles in controlling cancer development, is divided into antiapoptotic and proapoptotic members. The change in the balance between these members governs the life and death of the cells. Mcl-1 is an antiapoptotic member of this family and its distribution in normal and cancerous tissues strongly differs from that of Bcl-2. In human cancers, where upregulation of antiapoptotic proteins is common, Mcl-1 expression is regulated independent of Bcl-2 and its inhibition promotes senescence, a major barrier to tumorigenesis. Cancer chemotherapy determines various kinds of responses, such as senescence and autophagy; however, the ideal response to chemotherapy…

0301 basic medicineCarcinogenesisPhysiologyClinical BiochemistryApoptosisBiologymedicine.disease_causecancer care03 medical and health sciencesMcl-1 in cancer0302 clinical medicineBcl-2 familyimmune system diseasesCancer stem cellhemic and lymphatic diseasesNeoplasmsmedicinecancer-stem-cellHumansPost-translational regulationMolecular Targeted TherapyneoplasmsCellular SenescenceOncogeneBcl-2 familyAutophagyCancerCell Biologymedicine.diseaseMcl-1 isoformGene Expression Regulation Neoplastic030104 developmental biologyUSP9XProto-Oncogene Proteins c-bcl-2030220 oncology & carcinogenesisCancer researchtargeting Mcl-1Myeloid Cell Leukemia Sequence 1 ProteinCarcinogenesisProtein Processing Post-Translational
researchProduct

MYC-driven epigenetic reprogramming favors the onset of tumorigenesis by inducing a stem cell-like state

2018

Breast cancer consists of highly heterogeneous tumors, whose cell of origin and driver oncogenes are difficult to be uniquely defined. Here we report that MYC acts as tumor reprogramming factor in mammary epithelial cells by inducing an alternative epigenetic program, which triggers loss of cell identity and activation of oncogenic pathways. Overexpression of MYC induces transcriptional repression of lineage-specifying transcription factors, causing decommissioning of luminal-specific enhancers. MYC-driven dedifferentiation supports the onset of a stem cell-like state by inducing the activation of de novo enhancers, which drive the transcriptional activation of oncogenic pathways. Furthermo…

0301 basic medicineCarcinogenesisScienceGeneral Physics and AstronomyBreast NeoplasmsMice SCIDTumor initiationBiologyBreast cancer MYC Tumorigenesismedicine.disease_causeArticleGeneral Biochemistry Genetics and Molecular BiologyEpigenesis GeneticProto-Oncogene Proteins c-mycMice03 medical and health sciencesCell Line TumormedicineAnimalsHumansEpigeneticslcsh:ScienceEnhancerTranscription factorRegulation of gene expressionMultidisciplinaryQGeneral ChemistryCellular ReprogrammingCell biologyGene Expression Regulation NeoplasticEnhancer Elements Genetic030104 developmental biologyNeoplastic Stem CellsFemalelcsh:QStem cellCarcinogenesisReprogramming
researchProduct

Chemopreventive Property of Sencha Tea Extracts towards Sensitive and Multidrug-Resistant Leukemia and Multiple Myeloma Cells

2020

The popular beverage green tea possesses chemopreventive activity against various types of tumors. However, the effects of its chemopreventive effect on hematological malignancies have not been defined. In the present study, we evaluated antitumor efficacies of a specific green tea, sencha tea, on sensitive and multidrug-resistant leukemia and a panel of nine multiple myelomas (MM) cell lines. We found that sencha extracts induced cytotoxicity in leukemic cells and MM cells to different extents, yet its effect on normal cells was limited. Furthermore, sencha extracts caused G2/M and G0/G1 phase arrest during cell cycle progression in CCRF/CEM and KMS-12-BM cells, respectively. Specifically,…

0301 basic medicineCell Survivalnatural productsgreen tealcsh:QR1-502Cell morphologychemotherapyBiochemistryArticlelcsh:Microbiologyfunctional foodPhosphatidylinositol 3-Kinases03 medical and health sciences0302 clinical medicineCell Line TumorHumansCytotoxicityMolecular BiologyProtein kinase BcatechinsPI3K/AKT/mTOR pathwaypolyphenolsCell ProliferationMembrane Potential MitochondrialLeukemiadrug resistanceTeaPlant ExtractsChemistryCell growthCell CycleNF-kappa BCell cycleAntineoplastic Agents PhytogenicDrug Resistance MultipleGene Expression Regulation Neoplastic030104 developmental biologyDrug Resistance NeoplasmApoptosisCell culture030220 oncology & carcinogenesisflavonoidsCancer researchmicroarray analysisMultiple MyelomaReactive Oxygen SpeciesProto-Oncogene Proteins c-aktSignal TransductionBiomolecules
researchProduct

Synthesis and antiproliferative activity of a natural like glycoconjugate polycyclic compound

2016

Abstract A natural like O -glycoconjugate polycyclic compound 4 was obtained by a multistep procedure starting from N -(3-methyl-1-(4-nitrophenyl)-1 H -pyrazol-5-yl)acetamide. The glycosyl derivative 4 showed antiproliferative activity against all the tumoral cell lines of the NCI panel in the range 0.47–5.43  μ M. Cytofluorimetric analysis performed on MDA-MB231, a very aggressive breast cancer cell line, which does not express estrogen, progesterone and HER-2/neu receptors, showed that 4 is able to induce prolonged cell cycle arrest at G2/M phase and morphological signs of differentiation. These events are correlated with down-regulation of both cyclin B1 and cdc2, the cyclins involved in…

0301 basic medicineCell cycle checkpointCell SurvivalReceptor ErbB-2StereochemistryGlycoconjugateAntineoplastic AgentsAntiproliferative activityChemistry Techniques Synthetic03 medical and health sciences0302 clinical medicineCyclin-dependent kinaseCell Line TumorDrug DiscoveryHumansPolycyclic CompoundsMDA-MB231Cyclin B1Cell ProliferationCyclinPharmacologychemistry.chemical_classificationBiological ProductsCyclin-dependent kinase 1G2/M phase arrestp21WAF1 inhibitorbiologyChemistryKinaseDrug Discovery3003 Pharmaceutical ScienceO-glycoconjugate polycyclic compoundOrganic ChemistryGeneral MedicineMolecular biologyG2 Phase Cell Cycle CheckpointsGene Expression Regulation Neoplastic030104 developmental biologyCell culturePyrazolo[34-b]pyrazolo[3′4′:23]azepino[45-f]azocineDrug Design030220 oncology & carcinogenesisbiology.proteinM Phase Cell Cycle CheckpointsReceptors ProgesteroneGlycoconjugatesEuropean Journal of Medicinal Chemistry
researchProduct

EphrinB2 repression through ZEB2 mediates tumour invasion and anti-angiogenic resistance.

2016

Diffuse invasion of the surrounding brain parenchyma is a major obstacle in the treatment of gliomas with various therapeutics, including anti-angiogenic agents. Here we identify the epi-/genetic and microenvironmental downregulation of ephrinB2 as a crucial step that promotes tumour invasion by abrogation of repulsive signals. We demonstrate that ephrinB2 is downregulated in human gliomas as a consequence of promoter hypermethylation and gene deletion. Consistently, genetic deletion of ephrinB2 in a murine high-grade glioma model increases invasion. Importantly, ephrinB2 gene silencing is complemented by a hypoxia-induced transcriptional repression. Mechanistically, hypoxia-inducible facto…

0301 basic medicineCell signalingScienceGeneral Physics and AstronomyRepressorDown-RegulationAngiogenesis InhibitorsEphrin-B2BiologyGeneral Biochemistry Genetics and Molecular BiologyArticleNeovascularization03 medical and health sciencesDownregulation and upregulationddc:570GliomamedicineGene silencingAnimalsHumansNeoplasm InvasivenessPsychological repressionZinc Finger E-box Binding Homeobox 2Regulation of gene expressionMice KnockoutMultidisciplinaryNeovascularization PathologicQGeneral ChemistryGliomamedicine.diseaseHypoxia-Inducible Factor 1 alpha SubunitXenograft Model Antitumor AssaysCell HypoxiaCell biologyUp-RegulationBevacizumabGene Expression Regulation NeoplasticMice Inbred C57BL030104 developmental biologyDrug Resistance Neoplasmmedicine.symptomNature communications
researchProduct

CRISPR-Cas9 screen reveals a MYCN-amplified neuroblastoma dependency on EZH2.

2018

Pharmacologically difficult targets, such as MYC transcription factors, represent a major challenge in cancer therapy. For the childhood cancer neuroblastoma, amplification of the oncogene MYCN is associated with high-risk disease and poor prognosis. Here, we deployed genome-scale CRISPR-Cas9 screening of MYCN-amplified neuroblastoma and found a preferential dependency on genes encoding the polycomb repressive complex 2 (PRC2) components EZH2, EED, and SUZ12. Genetic and pharmacological suppression of EZH2 inhibited neuroblastoma growth in vitro and in vivo. Moreover, compared with neuroblastomas without MYCN amplification, MYCN-amplified neuroblastomas expressed higher levels of EZH2. ChIP…

0301 basic medicineCellular differentiationMedical and Health SciencesNeuroblastomaSUZ12Oncogene MYCNCRISPR-Cas SystemCancerPediatricNeuronsN-Myc Proto-Oncogene ProteinTumorEZH2EpigeneticCell DifferentiationGeneral MedicineUp-RegulationGene Expression Regulation NeoplasticOncology5.1 PharmaceuticalsEpigeneticsDevelopment of treatments and therapeutic interventionsHumanResearch ArticlePediatric Research InitiativePediatric CancerImmunologymacromolecular substancesBiologyN-Myc Proto-Oncogene ProteinCell Line03 medical and health sciencesRare DiseasesNeuroblastomaCell Line TumormedicineGeneticsHumansEnhancer of Zeste Homolog 2 ProteinTranscription factorneoplasmsNeoplasticHuman GenomeNeurosciencesGene AmplificationNeuronmedicine.disease030104 developmental biologyGene Expression RegulationCancer researchHistone deacetylaseCRISPR-Cas SystemsThe Journal of clinical investigation
researchProduct