Search results for " tumor suppressor"

showing 4 items of 64 documents

Loss of a novel tumor suppressor gene locus at chromosome 8p is associated with leukemic mantle cell lymphoma

2001

Abstract Patients with mantle cell lymphoma (MCL) may present with either nodal or leukemic disease. The molecular determinants underlying this different biologic behavior are not known. This study compared the pattern of genetic abnormalities in patients with nodal and leukemic phases of MCL using comparative genomic hybridization (CGH) and fluorescence in situ hybridization (FISH) for specific gene loci. Although both leukemic and nodal MCL showed similar genomic patterns of losses (involving 6q, 11q22-q23, 13q14, and 17p13) and gains (affecting 3q and 8q), genomic loss of chromosome 8p occurred more frequently in patients with leukemic disease (79% versus 11%,P < .001). Subsequent…

medicine.medical_specialtyTumor suppressor geneImmunologyGenes mycLocus (genetics)Lymphoma Mantle-CellBiologyBiochemistryMYC Gene AmplificationGene duplicationmedicineHumansGenes Tumor SuppressorIn Situ Hybridizationmedicine.diagnostic_testGene AmplificationCytogeneticsNucleic Acid HybridizationCell BiologyHematologyPrognosismedicine.diseaseCancer researchMantle cell lymphomaGene DeletionChromosomes Human Pair 8Fluorescence in situ hybridizationComparative genomic hybridizationBlood
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TP53 mutations and S-phase fraction but not DNA-ploidy are independent prognostic indicators in laryngeal squamous cell carcinoma

2005

To prospectively evaluate the prognostic significance of TP53, H-, K-, and N-Ras mutations, DNA-ploidy and S-phase fraction (SPF) in patients affected by locally advanced laryngeal squamous cell carcinoma (LSCC). Eight-one patients (median follow-up was 71 months) who underwent resective surgery for primary operable locally advanced LSCC were analyzed. Tumor DNA was screened for mutational analysis by PCR/SSCP and sequencing. DNA-ploidy and SPF were performed by flow cytometric analyses. Thirty-six patients (44%) had, at least, a mutation in the TP53 gene. Of them, 22% (8/36) had double mutations and 3% (1/36) had triple mutations. In total, 46 TP53 mutations were observed. The majority (41…

squamous cell carcinomasingle strand conformation polymorphismPrognosipolymerase chain reactionDNA Mutational AnalysisEMTREE drug terms: protein p53 EMTREE medical terms: advanced cancerS PhaseDNA Mutational AnalysiHumansprotein p53 advanced cancer; article; cell cycle S phase; DNA content; exon; flow cytometry; follow up; gene; gene mutation; genetic analysis; histopathology; human; human tissue; larynx carcinoma; multivariate analysis; ploidy; polymerase chain reaction; priority journal; prospective study; single strand conformation polymorphism; squamous cell carcinoma; tp53 gene Carcinoma Squamous Cell; DNA Mutational Analysis; DNA Neoplasm; Genes ras; Humans; Laryngeal Neoplasms; Mutation; Ploidies; Polymorphism Single-Stranded Conformational; Prognosis; S Phase; Survival Rate; Tumor Suppressor Protein p53 [EMTREE drug terms]follow uplarynx carcinomatp53 gene MeSH: Carcinoma Squamous Cellexongene mutationhumanmultivariate analysigeneLaryngeal NeoplasmsPolymorphism Single-Stranded ConformationalLaryngeal NeoplasmPloidiesflow cytometryarticleploidyDNA NeoplasmPrognosisGenes rahuman tissueSurvival RateGenes rascell cycle S phasepriority journalDNA contentgenetic analysiMutationCarcinoma Squamous CellhistopathologyTumor Suppressor Protein p53Ploidieprospective study
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Oncolytic targeting of renal cell carcinoma via encephalomyocarditis virus

2010

Apoptosis is a fundamental host defence mechanism against invading microbes. Inactivation of NF-kappaB attenuates encephalomyocarditis virus (EMCV) virulence by triggering rapid apoptosis of infected cells, thereby pre-emptively limiting viral replication. Recent evidence has shown that hypoxia-inducible factor (HIF) increases NF-kappaB-mediated anti-apoptotic response in clear-cell renal cell carcinoma (CCRCC) that commonly exhibit hyperactivation of HIF due to the loss of its principal negative regulator, von Hippel-Lindau (VHL) tumour suppressor protein. Here, we show that EMCV challenge induces a strong NF-kappaB-dependent gene expression profile concomitant with a lack of interferon-me…

virusesTransplantation HeterologousApoptosisMice SCIDBiologyNF-κBMice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineRNA interferenceCell Line TumorVHLEMCVBasic Helix-Loop-Helix Transcription FactorsAnimalsHIFEncephalomyocarditis virusRNA Small InterferingCarcinoma Renal CellResearch Articles030304 developmental biology0303 health sciencesNF-kappa BNF-κBNFKB1RCCVirologyKidney Neoplasms3. Good healthOncolytic virusOncolytic VirusesViral replicationchemistryVon Hippel-Lindau Tumor Suppressor ProteinApoptosisCell culture030220 oncology & carcinogenesisCancer researchMolecular MedicineRNA InterferenceSignal transductionSignal TransductionEMBO Molecular Medicine
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Clinical utility gene card for: von Hippel-Lindau (VHL).

2013

von Hippel-Lindau Diseasemedicine.diagnostic_testGenotypeVon Hippel-Lindau Tumor Suppressor ProteinBiologyVon hippel lindaumedicine.diseasePhenotypeCyclin D1PhenotypeVon Hippel-Lindau Tumor Suppressor ProteinGenotypeClinical Utility Gene CardGeneticsmedicineCancer researchHumansCyclin D1Genetic TestingVon Hippel–Lindau diseaseGeneGenetics (clinical)Genetic testingEuropean journal of human genetics : EJHG
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