0000000000756222

AUTHOR

Sylvia Mann

showing 5 related works from this author

Demethylation treatment restores hic1 expression and impairs aggressiveness of head and neck squamous cell carcinoma.

2010

Promoter hypermethylation of tumor suppressor genes is a common feature of primary cancer cells. However, at date the somatic epigenetic events that occur in head and neck squamous cell carcinoma (HNSCC) tumorigenesis are not yet been well defined. In the present study we analysed the methylation status of the gene hypermethylated in cancer-1 (hic1), a gene located on chromosome 17p13.3, a region frequently lost in HNSCC. We analysed 22 HNSCC samples and three cell lines using methylation specific PCR (MSP). We found hic1 methylated in 21 out of 22 samples and in all three cell lines. Treatment of the cell lines with the demethylating agent 5-Azacytidin (5-Aza) resulted in the demethylation…

AdultMaleCancer ResearchPathologymedicine.medical_specialtyAntimetabolites AntineoplasticTumor suppressor geneBisulfite sequencingKruppel-Like Transcription FactorsBiologymedicine.disease_causechemistry.chemical_compoundCell Line TumormedicineHumansGenes Tumor SuppressorNeoplasm InvasivenessPromoter Regions GeneticneoplasmsAgedMethylationDNA MethylationMiddle Agedmedicine.diseaseHead and neck squamous-cell carcinomaDemethylating agentGene Expression Regulation Neoplasticstomatognathic diseasesOncologychemistryEpidermoid carcinomaHead and Neck NeoplasmsCancer cellCancer researchAzacitidineCarcinoma Squamous CellFemaleOral SurgeryCarcinogenesisOral oncology
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Promoter methylation of MGMT, MLH1 and RASSF1A tumor suppressor genes in head and neck squamous cell carcinoma: Pharmacological genome demethylation …

2012

Promoter hypermethylation of tumor suppressor genes (TSGs) is a common feature of primary cancer cells. However, to date the somatic epigenetic events that occur in head and neck squamous cell carcinoma (HNSCC) tumorigenesis have not been well-defined. In the present study, we analyzed the promoter methylation status of the genes mutL homolog 1 (MLH1), Ras-association domain family member 1 (RASSF1A) and O-6-methylguanine-DNA methyltransferase (MGMT) in 23 HNSCC samples, three control tissues and one HNSCC cell line (UM-SCC 33) using methylation-specific PCR (MSP). The expression of the three proteins was quantified by semi-quantitative immunohistochemical analysis. The cell line was treate…

MaleCancer Researchmedicine.disease_causePolymerase Chain Reactionchemistry.chemical_compoundRas association domain family member 1Genes Tumor Suppressortumor suppressor geneEnzyme InhibitorsPromoter Regions GeneticDNA Modification MethylasesAged 80 and overNuclear ProteinsArticlesGeneral MedicineMethylationMiddle AgedImmunohistochemistryPrimary tumorOncologyDealkylationHead and Neck NeoplasmsDNA methylationAzacitidineCarcinoma Squamous CellFemaleMutL Protein Homolog 1Molecular Sequence DataDown-RegulationBiologyhead and neck squamous cell carcinomamutL homolog 15-azacytidineCell Line TumormedicineHumansEpigeneticsneoplasmsO-6-methylguanine-DNA methyltransferaseAdaptor Proteins Signal TransducingAgedCell ProliferationBase SequenceDose-Response Relationship DrugTumor Suppressor ProteinsSequence Analysis DNADNA Methylationmedicine.diseaseHead and neck squamous-cell carcinomaMolecular biologyDemethylating agentSquamous carcinomastomatognathic diseasesDNA Repair EnzymeschemistryCase-Control StudiesCpG IslandsCarcinogenesisOncology Reports
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Pharmacological genome demethylation increases radiosensitivity of head and neck squamous carcinoma cells

2011

Aberrant inactivation of tumor suppressor genes by promoter hypermethylation has been recognized as a crucial step of tumor development and is related to aggressiveness and therapy resistance. To identify potential novel treatment strategies, we evaluated pharmacological genome demethylation for the increase of irradiation treatment effectiveness in head and neck squamous cell carcinoma (HNSCC) in this in vitro study. HNSCC cells were cultured with 2 different concentrations of 5-azacytidine (5-Aza) for 72 h, followed by a single fraction irradiation with 4 or 50 Gy, respectively. To show successful genome demethylation, the methylation status of the tumor suppressor gene hic1 (hypermethyla…

Transcriptional ActivationAntimetabolites AntineoplasticTumor suppressor geneBisulfite sequencingBiologyRadiation ToleranceCell Line TumorGeneticsmedicineHumansRadiosensitivityPromoter Regions GeneticDemethylationOncogeneSquamous Cell Carcinoma of Head and NeckGeneral MedicineDNA MethylationCell cyclemedicine.diseaseHead and neck squamous-cell carcinomaSquamous carcinomaGene Expression Regulation NeoplasticHead and Neck NeoplasmsAzacitidineCarcinoma Squamous CellCancer researchInternational Journal of Molecular Medicine
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Assessment of determinants affecting the dual topology of hepadnaviral large envelope proteins

2004

For functional diversity, the large (L) envelope protein of hepatitis B virus (HBV) acquires a dual transmembrane topology via co-translational membrane integration of the S region and partial post-translational translocation of the preS subdomain. Because each process requires the second transmembrane segment (TM2), we explored the action of this determinant by using protease protection analysis of mutant L proteins. We demonstrated that neither the disruption of a leucine zipper-like motif by multiple alanine substitutions nor the flanking charges of TM2 affected the topological reorientation of L. The dispensability of both putative subunit interaction modules argues against a link betwe…

AlanineHepatitis B virusHepatitis B virusVirus AssemblyAmino Acid MotifsMolecular Sequence DataProtein domainPhenotype mixingBiological TransportBiologyEndoplasmic Reticulummedicine.disease_causeVirologyTransmembrane domainDual topologyAmino Acid SubstitutionViral Envelope ProteinsVirologyMembrane topologymedicineHepadnavirusAmino Acid SequenceProtein Processing Post-TranslationalJournal of General Virology
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γ2-Adaptin, a Novel Ubiquitin-interacting Adaptor, and Nedd4 Ubiquitin Ligase Control Hepatitis B Virus Maturation

2006

Hepatitis B virus (HBV) budding from infected cells is a tightly regulated process that requires both core and envelope structures. Here we report that HBV uses cellular γ2-adaptin and Nedd4, possibly in conjunction with ubiquitin, to coordinate its assembly and release. In search of interaction partners of the viral L envelope protein, we previously discovered γ2-adaptin, a putative endosomal sorting and trafficking adaptor of the adaptor protein complex family. We now demonstrate that the viral core interacts with the same γ2-adaptor and that disruption of the HBV/γ2-adaptin interactions inhibits virus production. Mutational analyses revealed a hitherto unknown ubiquitin-binding activity …

Hepatitis B virusbiologyEndosomeSignal transducing adaptor proteinDNA virusNEDD4Cell Biologymedicine.disease_causeBiochemistryMolecular biologyProtein ubiquitinationUbiquitin ligaseUbiquitinbiology.proteinmedicineMolecular BiologyJournal of Biological Chemistry
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