Search results for "sequence"

showing 10 items of 4987 documents

Chemotherapy-induced apoptosis in hepatocellular carcinoma involves the p53 family and is mediatedviathe extrinsic and the intrinsic pathway

2010

We investigated the downstream mechanisms by which chemotherapeutic drugs elicit apoptosis in hepatocellular carcinoma (HCC). Genomic signatures of HCC cell lines treated with different chemotherapeutic drugs were obtained. Analyses of apoptosis pathways were performed and RNA interference was used to evaluate the role of the p53 family. Endogenous p53, p63 and p73 were upregulated in response to DNA damage by chemotherapeutic drugs. Blocking p53 family function led to chemoresistance in HCC. Stimulation and blocking experiments of the CD95-, the TNF- and the TRAIL-receptor systems revealed that cytotoxic drugs, via the p53 family members as transactivators, can trigger expression of each o…

Cancer ResearchProgrammed cell deathCarcinoma HepatocellularTumor suppressor geneDNA damagetumor suppressor protein p53membrane proteinsoligonucleotide array sequence analysiscarcinomaBiologyhepatocellularfas-associated death domain proteinAPAF1humansMembrane Potential Mitochondrialhep G2 cellsbleomycinliver neoplasmsSettore BIO/11apoptosisPrognosismitochondrialFas receptorcaspasesOncologyApoptosisbiology.proteinCancer researchMdm2membrane potentialSignal transductionPrognosis; bleomycin; caspases; membrane potential mitochondrial; oligonucleotide array sequence analysis; tumor suppressor protein p53; membrane proteins; fas-associated death domain protein; humans; liver neoplasms; hep G2 cells; apoptosis; carcinoma hepatocellularInternational Journal of Cancer
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Identification and validation of novel ERBB2 (HER2, NEU) targets including genes involved in angiogenesis.

2005

V-erb-b2 erythroblastic leukemia viral oncogene homolog 2 (ERBB2; synonyms HER2, NEU) encodes a transmembrane glycoprotein with tyrosine kinase-specific activity that acts as a major switch in different signal-transduction processes. ERBB2 amplification and overexpression have been found in a number of human cancers, including breast, ovary and kidney carcinoma. Our aim was to detect ERBB2-regulated target genes that contribute to its tumorigenic effect on a genomewide scale. The differential gene expression profile of ERBB2-transfected and wild-type mouse fibroblasts was monitored employing DNA microarrays. Regulated expression of selected genes was verified by RT-PCR and validated by West…

Cancer ResearchReceptor ErbB-2Blotting WesternViral OncogeneDown-RegulationComputational biologyBiologymedicine.disease_causeTransfectionGenomeMiceGene expressionmedicineAnimalsHumansskin and connective tissue diseasesGeneDNA PrimersGlycoproteinsOligonucleotide Array Sequence AnalysisGeneticsRegulation of gene expressionGenomeNeovascularization PathologicReverse Transcriptase Polymerase Chain ReactionFibroblastsGenes erbB-2Up-RegulationGene expression profilingGene Expression Regulation NeoplasticCell Transformation NeoplasticOncologyNIH 3T3 CellsDNA microarrayCarcinogenesisSignal TransductionInternational journal of cancer
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ERBB2 Induces an Antiapoptotic Expression Pattern of Bcl-2 Family Members in Node-Negative Breast Cancer

2010

AbstractPurpose: Members of the Bcl-2 family act as master regulators of mitochondrial homeostasis and apoptosis. We analyzed whether ERBB2 influences the prognosis of breast cancer by influencing the proapoptotic versus antiapoptotic balance of Bcl-2 family members.Experimental Design: ERBB2-regulated Bcl-2 family members were identified by inducible expression of ERBB2 in MCF-7 breast cancer cells and by correlation analysis with ERBB2 expression in breast carcinomas. The prognostic relevance of ERBB2-regulated and all additional Bcl-2 family members was determined in 782 patients with untreated node-negative breast cancer. The biological relevance of ERBB2-induced inhibition of apoptosis…

Cancer ResearchReceptor ErbB-2Transplantation HeterologousMedizinApoptosisBreast NeoplasmsBiologyBioinformaticsModels BiologicalBAG1Cohort StudiesMiceBreast cancerDownregulation and upregulationTumor Cells CulturedmedicineAnimalsHumansskin and connective tissue diseasesOligonucleotide Array Sequence AnalysisClusterinGene Expression ProfilingCarcinomaBcl-2 familyCancermedicine.diseaseGenes bcl-2Gene Expression Regulation NeoplasticTransplantationOncologyMultigene FamilyBCL2L13NIH 3T3 CellsCancer researchbiology.proteinFemaleLymph NodesApoptosis Regulatory ProteinsClinical Cancer Research
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Novel recombinant GII.P16_GII.13 and GII.P16_GII.3 norovirus strains in Italy.

2014

Novel norovirus strains are continuously emerging worldwide. Molecular investigation and phylogenetic analysis identified GII.P16 recombinant noroviruses from the stools of four Italian children with gastroenteritis. The capsid gene was characterized as either GII.13 or GII.3. The GII.P16_GII.13 Italian strains were closely related to German strains involved in a large outbreak in the second half of 2012 and the Italian strains are the first recorded occurrence of GII.P16_GII.13 in Europe.

Cancer ResearchSettore MED/07 - Microbiologia E Microbiologia ClinicaGenotypevirusesMolecular Sequence DataBiologymedicine.disease_causelaw.inventionfluids and secretionslawVirologymedicineCluster AnalysisHumansGenePhylogenyCaliciviridae InfectionsRecombination GeneticNoroviruPhylogenetic treeGastroenteritiNorovirusvirus diseasesOutbreakGII.P16_GII.3InfantSequence Analysis DNAVirologyRecombinationGastroenteritisInfectious DiseasesCapsidItalyChild PreschoolRecombinant DNANorovirusRNA ViralCapsid ProteinsGII.P16_GII.13Virus research
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Geographical distribution and oncogenic risk association of human papillomavirus type 58 E6 and E7 sequence variations.

2013

Human papillomavirus (HPV) 58 accounts for a notable proportion of cervical cancers in East Asia and parts of Latin America, but it is uncommon elsewhere. The reason for such ethnogeographical predilection is unknown. In our study, nucleotide sequences of E6 and E7 genes of 401 HPV58 isolates collected from 15 countries/cities across four continents were examined. Phylogenetic relationship, geographical distribution and risk association of nucleotide sequence variations were analyzed. We found that the E6 genes of HPV58 variants were more conserved than E7. Thus, E6 is a more appropriate target for type-specific detection, whereas E7 is more appropriate for strain differentiation. The frequ…

Cancer ResearchSettore MED/07 - Microbiologia E Microbiologia Clinicacervical cancerSettore MED/06 - Oncologia MedicaPapillomavirus E7 ProteinsUterine Cervical NeoplasmsCervix UteriphylogenyPolymerase Chain ReactionViralPapillomaviridaePapillomaviridaePhylogenyCancerOncogene ProteinsCervical cancerGeneticsTumorGeographybiologyNucleic acid sequenceDNA NeoplasmPrognosisInfectious DiseasesOncologyHIV/AIDSFemaleHPVhuman papillomavirus type 58 E6 and E7 sequence variationsOncology and CarcinogenesisCervical intraepithelial neoplasiaRisk AssessmentArticleVaccine Relatedoncogenic riskClinical ResearchPhylogeneticsGenetic variationGeneticsBiomarkers TumormedicineHumansOncology & CarcinogenesisGenePreventionPapillomavirus InfectionsGenetic VariationInternational AgenciesDNAOncogene Proteins ViralOdds ratioUterine Cervical Dysplasiamedicine.diseasebiology.organism_classificationVirologyvariantNeoplasmSexually Transmitted InfectionsCapsid ProteinsBiomarkersFollow-Up Studies
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Differential MHC class II component expression in HPV-positive cervical cancer cells: implication for immune surveillance.

2005

Effective eradication of human papillomavirus (HPV)-positive tumors may require CD8+ and CD4+ T-cell-mediated immune responses. Ectopic expression of MHC class II surface molecules has been described in the context of cervical cancer, but coexpression with other components of the MHC class II antigen presentation pathway has not been addressed. We have evaluated the MHC class II antigen presentation pathway in malignant squamous epithelium of HPV+ cervical cancer lesions by in situ costaining HLA-DR with CLIP or DMA/DMB. Cervical cancer cells exhibit 3 MHC class II phenotypes: (i) DR+/CLIP+ or DM+; (ii) DR+/CLIP- or DM-; and (iii) DR-/CLIP+ or DM+. The identical profile has been identified …

Cancer ResearchT cellT-LymphocytesFluorescent Antibody TechniqueUterine Cervical NeoplasmsEnzyme-Linked Immunosorbent AssayMHC class II antigenInterferon-gammaAntigenMHC class ImedicineHumansPapillomaviridaeDNA PrimersMHC class IIbiologyBase SequenceAntigen processingReverse Transcriptase Polymerase Chain ReactionHistocompatibility Antigens Class IIMHC restrictionmedicine.anatomical_structureOncologyImmunologybiology.proteinFemaleCD8International journal of cancer
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The FHIT gene is alternatively spliced in normal kidney and renal cell carcinoma.

1997

FHIT (Fragile Histidine Triad), a putative tumor suppressor gene, was cloned from fetal brain and colon cDNA libraries. Portions of this gene are deleted in esophageal, colon, lung and breast tumors, but this gene has not been found altered in sporadic renal cell carcinomas. We report here an alternatively spliced form of this gene cloned from a kidney cDNA library. This cDNA is 1189 bp in length, and contains an additional 94 bp exon, designated exon 2a (E2a). This novel sequence is located between exon 2 and exon 3 of the FHIT gene's untranslated region and exon 2a is present in all normal kidney tissues and cell lines. Analyses performed on sporadic renal cell carcinoma (RCC) tissues and…

Cancer ResearchTumor suppressor geneMolecular Sequence DataBiologymedicine.disease_causeKidneyPolymerase Chain ReactionExonFHITComplementary DNAGene expressionGeneticsmedicineHumansGenes Tumor SuppressorAmino Acid SequenceCloning MolecularneoplasmsMolecular BiologyCarcinoma Renal CellBase SequencecDNA libraryAlternative splicingProteinsBlotting NorthernKidney NeoplasmsAcid Anhydride HydrolasesNeoplasm ProteinsAlternative SplicingCancer researchCarcinogenesisOncogene
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cDNA sequences of the authentic keratins 8 and 18 in zebrafish

2003

From the zebrafish Danio rerio, we have cDNA cloned and sequenced a novel type II and a novel type I keratin, termed DreK8 and DreK18, respectively. We identified DreK8/18 as the true orthologs of the human keratin pair K8/18 as follows: (i) MALDI-MS assignment to the biochemically identified K8 and K18 candidates that are co-expressed in simple epithelia and absent in epidermal keratinocytes; (ii) multiple sequence alignments and phylogenetic tree analysis, showing that DreK8, within the phylogenetic tree of type II keratins, forms a highly bootstrap-supported branch together with K8 from goldfish and rainbow trout, whereas DreK18, within the phylogenetic tree of type I keratins, groups wi…

Cancer Researchanimal structuresType I keratinMolecular Sequence DataDaniomacromolecular substancesBiologyType II keratinComplementary DNAKeratinAnimalsHumansTissue DistributionAmino Acid SequenceCloning MolecularMolecular BiologyZebrafishPhylogenyZebrafishGeneticschemistry.chemical_classificationKeratin-18integumentary systemPhylogenetic treeKeratin-8Nucleic acid sequenceCell BiologyZebrafish Proteinsbiology.organism_classificationchemistryKeratinsSequence AlignmentDevelopmental BiologyDifferentiation
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Tracheal development and the von Hippel-Lindau tumor suppressor homolog in Drosophila.

2000

von Hippel-Lindau disease is a hereditary cancer syndrome. Mutations in the VHL tumor suppressor gene predispose individuals to highly vascularized tumors. However, VHL-deficient mice die in utero due to a lack of vascularization in the placenta. To resolve the contradiction, we cloned the Drosophila VHL homologue (d-VHL) and studied its function. It showed an overall 50% similarity to the human counterpart and 76% similarity in the crucial functional domain: the elongin C binding site. The putative d-VHL protein can bind Drosophila elongin C in vitro. During embryogenesis, d-VHL is expressed in the developing tracheal regions where tube outgrowth no longer occurs. Reduced d-VHL activity (u…

Cancer Researchendocrine system diseasesTumor suppressor geneUbiquitin-Protein LigasesMolecular Sequence Dataurologic and male genital diseasesTube fusionLigasesRNA interferenceVon Hippel–Lindau tumor suppressorGeneticsmedicineAnimalsHumansGenes Tumor SuppressorAmino Acid SequenceVon Hippel–Lindau diseaseCloning MolecularneoplasmsMolecular BiologyGeneticsbiologyTumor Suppressor ProteinsProteinsCell migrationEmbryomedicine.diseasePhenotypefemale genital diseases and pregnancy complicationsCell biologyTracheaPhenotypeVon Hippel-Lindau Tumor Suppressor Proteinbiology.proteinDrosophilaOncogene
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Mammary-derived growth inhibitor (MDGI) interacts with integrin α-subunits and suppresses integrin activity and invasion

2010

The majority of mortality associated with cancer is due to formation of metastases from the primary tumor. Adhesion mediated by different integrin heterodimers has an important role during cell migration and invasion. Protein interactions with the β1-integrin cytoplasmic tail are known to influence integrin affinity for extracellular ligands, but regulating binding partners for the α-subunit cytoplasmic tails have remained elusive. In this study, we show that mammary-derived growth inhibitor (MDGI) (also known as FABP-3 or H-FABP) binds directly to the cytoplasmic tail of integrin α-subunits and its expression inhibits integrin activity. In breast cancer cell lines, MDGI expression correlat…

Cancer Researchmedicine.disease_causemigrationCD49cCollagen receptor0302 clinical medicineCell Movement0303 health sciencesCell migrationMiddle Agedinvasion3. Good healthCell biologyExtracellular MatrixadhesionIntegrin alpha MMDGI030220 oncology & carcinogenesis/dk/atira/pure/sustainabledevelopmentgoals/good_health_and_well_beingIntegrin beta 6FemaleFatty Acid Binding Protein 3Integrin alpha Chainsmedicine.medical_specialtyintegrinIntegrinMolecular Sequence DataBreast NeoplasmsBiologyFatty Acid-Binding ProteinsCollagen Type IDisease-Free Survival03 medical and health sciencesbreast cancerSDG 3 - Good Health and Well-beingInternal medicineCell Line TumorGeneticsmedicineHumansNeoplasm InvasivenessProtein Interaction Domains and MotifsAmino Acid SequenceMolecular Biology030304 developmental biologyFibronectinsFibronectinEndocrinologybiology.proteinCarcinogenesisOncogene
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