Search results for "oncogene"

showing 10 items of 1005 documents

Analysis of biological prognostic factors using tissue microarrays in neuroblastic tumors

2009

Background Neuroblastic tumors (NT) are pediatric neoplasms with a heterogeneous genetic profile. They present genotypic alterations of prognostic value, the study of which is mandatory in designing therapeutic management. Tissue microarrays (TMA) from paraffin material allow the analysis of a large number of cases with minimal costs. The main purpose of the present study is to analyze specific genetic markers of neuroblastic tumors included in TMAs and determine their prognostic value. We compare the results obtained by different molecular techniques at different substrates to evaluate the feasibility of these assays. Procedure One hundred thirty-nine samples were included in four differen…

Genetic MarkersMalePathologymedicine.medical_specialtyDiseaseN-Myc Proto-Oncogene ProteinNeuroblastomaRisk FactorsGenotypeHumansMedicineStage (cooking)ChildRetrospective StudiesOncogene ProteinsN-Myc Proto-Oncogene ProteinTissue microarraybusiness.industryAge FactorsNuclear ProteinsCell DifferentiationRetrospective cohort studyHematologyPrognosisNeuroblastic TumorTreatment OutcomeOncologyTissue Array AnalysisGenetic markerMutationPediatrics Perinatology and Child HealthFemalebusinessPediatric Blood & Cancer
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TET2 mutation is an independent favorable prognostic factor in myelodysplastic syndromes (MDSs).

2009

Abstract Oncogenic pathways underlying in the development of myelodysplastic syndromes (MDS) remain poorly characterized, but mutations of the ten-eleven translocation 2 (TET2) gene are frequently observed. In the present work, we evaluated the prognostic impact of TET2 mutations in MDS. Frameshift, nonsense, missense mutations, or defects in gene structure were identified in 22 (22.9%) of 96 patients (95% confidence interval [CI], 14.5-31.3 patients). Mutated and unmutated patients did not significantly differ in initial clinical or hematologic parameters. The 5-year OS was 76.9% (95% CI, 49.2%-91.3%) in mutated versus 18.3% (95% CI, 4.2%-41.1%) in unmutated patients (P = .005). The 3-year…

Genetic MarkersMalemedicine.medical_specialtyPathologyImmunologyBiochemistryGastroenterologyDisease-Free SurvivalFrameshift mutationDioxygenasesPredictive Value of TestsRisk FactorsInternal medicineProto-Oncogene ProteinsmedicineMissense mutationHumansAgedAged 80 and overUnivariate analysisProportional hazards modelbusiness.industryMyelodysplastic syndromesHazard ratioCell BiologyHematologyMiddle Agedmedicine.diseaseConfidence intervalDNA-Binding ProteinsSurvival RateInternational Prognostic Scoring SystemMyelodysplastic SyndromesMutationFemalebusinessFollow-Up StudiesBlood
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Comparative architectural aspects of regions of conserved synteny on human chromosome 11p15.3 and mouse chromosome 7 (including genes WEE1 and LMO1)

2001

Human chromosome 11p15.3 is associated with chromosome aberrations in the Beckwith Wiedemann Syndrome and implicated in the pathogenesis of different tumor types including lung cancer and leukemias. To date, only single tumor-relevant genes with linkage to this region (e.g. LMO1) have been found suggesting that this region may harbor additional potential disease associated genes. Although this genomic area has been studied for years, the exact order of genes/chromosome markers between D11S572 and the WEE1 gene locus remained unclear. Using the FISH technique and PAC clones of the flanking markers we determined the order of the genomic markers. Based on these clones we established a PAC cont…

Genetic Markerscongenital hereditary and neonatal diseases and abnormalitiesBeckwith–Wiedemann syndromeCell Cycle ProteinsBiologyChromosomesEvolution MolecularContig MappingMiceChromosome regionsGene OrderMetalloproteinsGeneticsmedicineAnimalsHumansCloning MolecularMolecular BiologyGeneConserved SequenceIn Situ Hybridization FluorescenceGenetics (clinical)Repetitive Sequences Nucleic AcidSyntenyOncogene ProteinsGeneticsChromosome 7 (human)Base CompositionChromosomes Human Pair 11Nuclear ProteinsChromosomeSequence Analysis DNALIM Domain ProteinsProtein-Tyrosine Kinasesmedicine.diseaseAT Rich SequenceGC Rich SequenceDNA-Binding ProteinsChromosome 3CpG IslandsChromosome 21Transcription FactorsCytogenetic and Genome Research
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Who has to undergo cancer genetic testing? A perspective

2017

Genetic testing is a medical tool employed to screen changes in genes linked to cancer and other genetic diseases. Genetic tests are available for breast, ovarian, colon, thyroid, and some other cancers and they represent the main tool for early identification of the “risk” subjects. The choice to undergo genetic testing by a healthy or affected cancer patient with family history of the cancer has to be the fruit of a careful and prudent assessment of the advantages and disadvantages discussed during oncogenetic counselling. The latter, in turn, in the case of a patient’s positive and informed choice, must constantly affiliate the genetic testing, in order to preserve the prediction and inf…

Genetic testingOncogenetic counsellingMedicine (all)Cancer
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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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Drp1 Controls Effective T Cell Immune-Surveillance by Regulating T Cell Migration, Proliferation, and cMyc-Dependent Metabolic Reprogramming

2018

Summary Mitochondria are key players in the regulation of T cell biology by dynamically responding to cell needs, but how these dynamics integrate in T cells is still poorly understood. We show here that the mitochondrial pro-fission protein Drp1 fosters migration and expansion of developing thymocytes both in vitro and in vivo. In addition, we find that Drp1 sustains in vitro clonal expansion and cMyc-dependent metabolic reprogramming upon activation, also regulating effector T cell numbers in vivo. Migration and extravasation defects are also exhibited in Drp1-deficient mature T cells, unveiling its crucial role in controlling both T cell recirculation in secondary lymphoid organs and acc…

Genetics and Molecular Biology (all)0301 basic medicinecell migrationT-LymphocytesCellCell CountMitochondrionLymphocyte ActivationBiochemistryCell MovementHomeostasismetabolic reprogrammingcell migration; cell proliferation; cMyc; Drp1; exhaustion; metabolic reprogramming; mitochondrial dynamics; T cells; thymocytes; tumor immune-surveillance; Biochemistry Genetics and Molecular Biology (all)lcsh:QH301-705.5cMycImmunologic SurveillanceMice KnockoutThymocytesEffectorDrp1; T cells; cMyc; cell migration; cell proliferation; exhaustion; metabolic reprogramming; mitochondrial dynamics; thymocytes; tumor immune-surveillanceCell migrationCell DifferentiationCell biologymedicine.anatomical_structurePhenotypeDynaminsendocrine systemSettore BIO/06Cell SurvivalLymphoid TissueMAP Kinase Signaling SystemT cellT cellsReceptors Antigen T-CellDrp1BiologyGeneral Biochemistry Genetics and Molecular BiologyArticleProto-Oncogene Proteins c-myc03 medical and health sciencestumor immune-surveillancemitochondrial dynamicexhaustionHomeostasimedicineAnimalsCell ProliferationTumor microenvironmentBiochemistry Genetics and Molecular Biology (all)Cell growthAnimalT cellthymocytemitochondrial dynamicsDynamin030104 developmental biologylcsh:Biology (General)T-LymphocyteT cell migration
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The Clinical Significance of Unknown Sequence Variants in BRCA Genes.

2010

Abstract: Germline mutations in BRCA1/2 genes are responsible for a large proportion of hereditary breast and/or ovarian cancers. Many highly penetrant predisposition alleles have been identified and include frameshift or nonsense mutations that lead to the translation of a truncated protein. Other alleles contain missense mutations, which result in amino acid substitution and intronic variants with splicing effect. The discovery of variants of uncertain/unclassified significance (VUS) is a result that can complicate rather than improve the risk assessment process. VUSs are mainly missense mutations, but also include a number of intronic variants and in-frame deletions and insertions. Over …

GeneticsCancer ResearchBRCA genesNonsense mutationReviewBiologylcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogenslcsh:RC254-282oncogenetic counselingFrameshift mutationintegrated modelsGermline mutationOncologyvariantRNA splicingMissense mutationClinical significanceAlleleGeneCancers
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Cancer stem cells – old concepts, new insights

2008

Cancer has long been viewed as an exclusively genetic disorder. The model of carcinogenesis, postulated by Nowell and Vogelstein, describes the formation of a tumor by the sequential accumulation of mutations in oncogenes and tumor suppressor genes. In this model, tumors are thought to consist of a heterogeneous population of cells that continue to acquire new mutations, resulting in a highly dynamic process, with clones that out compete others due to increased proliferative or survival capacity. However, novel insights in cancer stem cell research suggest another layer of complexity in the process of malignant transformation and preservation. It has been reported that only a small fraction…

GeneticsCell typeCancerOncogenesCell BiologyBiologymedicine.diseasemedicine.disease_causeMalignant transformationTransplantationMiceCancer stem cellHematologic NeoplasmsNeoplasmsGenetic modelCancer cellNeoplastic Stem CellsmedicineCancer researchAnimalsHumansNeoplasm MetastasisCarcinogenesisMolecular BiologyCell Death & Differentiation
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Next generation sequencing of HCC from European and Asian HCC cohorts. Back to p53 and Wnt/β-catenin

2013

Hepatocellular carcinoma (HCC) is the most common pri- mary liver malignancy. Here, we performed high-resolution copy- number analysis on 125 HCC tumors and whole-exome sequencing on 24 of these tumors. We identified 135 homozygous deletions and 994 somatic mutations of genes with predicted functional conse- quences. We found new recurrent alterations in four genes (ARID1A, RPS6KA3, NFE2L2 and IRF2) not previously described in HCC. Func- tional analyses showed tumor suppressor properties for IRF2, whose inactivation, exclusively found in hepatitis B virus (HBV)-related tumors, led to impaired TP53 function. In contrast, inactivation of chromatin remodelers was frequent and predominant in al…

GeneticsHepatitis B virusARID1AOncogeneTumor suppressor geneHepatologyHCCSBiologymedicine.disease_causemedicine.diseaseGermline mutationHepatocellular carcinomamedicineCancer researchCarcinogenesisJournal of Hepatology
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Identification and prevention of genotyping errors caused by G-quadruplex- and i-motif-like sequences.

2009

Abstract Background: Reliable PCR amplification of DNA fragments is the prerequisite for most genetic assays. We investigated the impact of G-quadruplex– or i-motif–like sequences on the reliability of PCR-based genetic analyses. Methods: We found the sequence context of a common intronic polymorphism in the MEN1 gene (multiple endocrine neoplasia I) to be the cause of systematic genotyping errors by inducing preferential amplification of one allelic variant [allele dropout (ADO)]. Bioinformatic analyses and pyrosequencing-based allele quantification enabled the identification of the underlying DNA structures. Results: We showed that G-quadruplex– or i-motif–like sequences can reproducibly …

GeneticsdbSNPBase SequenceGenotypeBiochemistry (medical)Clinical BiochemistrySingle-nucleotide polymorphismDNABiologyPolymerase Chain ReactionPolymorphism Single Nucleotidelaw.inventionG-QuadruplexeslawProto-Oncogene ProteinsGenotypeOMIM : Online Mendelian Inheritance in ManAlleleGeneGenotypingPolymerase chain reactionClinical chemistry
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