Search results for "Base Sequence"

showing 10 items of 1146 documents

Chimeric amplicons containing the c-myc gene in HL60 cells

1998

The major amplicon present in HL60 cells is chimeric in nature being composed of 70 kb of DNA sequence derived from the MYC locus linked to 80 kb of novel DNA sequence derived from a non contiguous region located telomeric to the c-myc gene at 8q24 (Feo et al., 1996). Here we show by fluorescence in situ hybridization (FISH) that these coamplified sequences, MCR (Myc Coamplified Region), are derived from a locus located 3-4 Mb telomeric to the c-myc gene in the q24.2-24.3 region of chromosome 8. Genomic cloning and Southern blot analysis indicate the arrangement of chimeric amplicons are in tandem arrays. Analysis of the DNA sequences at the juncture of the MYC locus and the MCR suggest tha…

Cancer ResearchOncogene Proteins FusionInverted repeatMolecular Sequence DataGenes mycHL-60 CellsLocus (genetics)BiologyMolecular cloningDNA sequencingLeukemia Promyelocytic AcuteGene mappingGeneticsHumansCloning MolecularMolecular BiologyGeneIn Situ Hybridization FluorescenceSouthern blotChromosome AberrationsRecombination GeneticGeneticsBase SequenceChromosome FragilityGene AmplificationSequence Analysis DNAAmpliconMolecular biologyBlotting SouthernChromosomes Human Pair 8Oncogene
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EWS/FLI-1 rearrangement in small round cell sarcomas of bone and soft tissue detected by reverse transcriptase polymerase chain reaction amplificatio…

1994

Recent cloning of the t(11;22) region has led to the detection of a number of sequences involved in the breakpoints by substituting a sequence which encodes a putative RNA binding domain for that of the DNA binding domain of the human homologue of murine FLI-1. Several tumours display consistent translocation at t(11;22) (q24;q12), a finding that suggests these fusion transcripts could be expressed and detected by reverse transcriptase polymerase chain reaction amplification. To date, only a small number of Ewing's sarcomas (Es) and peripheral neuroectodermal tumours (pPNET) of bone have been tested with this novel molecular biology approach. In this study, we confirmed the presence of the …

Cancer ResearchPathologymedicine.medical_specialtyChromosomes Human Pair 22Molecular Sequence DataTransplantation HeterologousEctomesenchymomaMice NudeBone NeoplasmsSoft Tissue NeoplasmsSarcoma EwingBone SarcomaBiologyPolymerase Chain ReactionTranslocation GeneticMiceProto-Oncogene ProteinsmedicineAnimalsHumansNeuroectodermal tumorBase SequenceProto-Oncogene Protein c-fli-1Soft tissue sarcomaChromosomes Human Pair 11Ewing's sarcomaRNA-Directed DNA PolymeraseGene rearrangementmedicine.diseaseDNA-Binding ProteinsReal-time polymerase chain reactionOncologySarcoma Small CellCancer researchTrans-ActivatorsOsteosarcomaEuropean journal of cancer (Oxford, England : 1990)
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De novo expression of intercellular adhesion molecule 1 (ICAM-1, CD54) in pancreas cancer.

1993

We examined the expression of intercellular--adhesion molecule-I (ICAM-I, CD54) in 6 surgically removed pancreatic tumors and 8 pancreatic tumor cell lines. Immunohistochemistry revealed a varying percentage of ICAM-I-positive pancreas tumor cells, while normal pancreatic tissue (except for slight reactivity of endothelial cells) was not stained. The presence of the ICAM-I molecule on the cell surface and the expression of ICAM-I mRNA were investigated for 8 different pancreatic tumor cell lines. Three of these (Capan-I, Capan-2, QGP-I) expressed ICAM-I constitutively. In 4 of the ICAM-I-negative pancreas cancer cell lines, it was possible to induce a remarkable expression of ICAM-I by incu…

Cancer ResearchPathologymedicine.medical_specialtyPancreatic diseaseCellMolecular Sequence DataBiologyProinflammatory cytokineImmunoenzyme TechniquesPancreatic tumorAntigens CDmedicineTumor Cells CulturedHumansRNA MessengerRNA NeoplasmBase SequenceCell adhesion moleculeCancermedicine.diseaseIntercellular Adhesion Molecule-1Molecular biologyPancreatic Neoplasmsmedicine.anatomical_structureOncologyCell culturePancreasCell Adhesion MoleculesInternational journal of cancer
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Claudin-18 splice variant 2 is a pan-cancer target suitable for therapeutic antibody development

2008

Abstract Purpose: Antibody-based cancer therapies have emerged as the most promising therapeutics in oncology. The purpose of this study was to discover novel targets for therapeutic antibodies in solid cancer. Experimental Design: We combined data mining and wet-bench experiments to identify strictly gastrocyte lineage–specific cell surface molecules and to validate them as therapeutic antibody targets. Results: We identified isoform 2 of the tight junction molecule claudin-18 (CLDN18.2) as a highly selective cell lineage marker. Its expression in normal tissues is strictly confined to differentiated epithelial cells of the gastric mucosa, but it is absent from the gastric stem cell zone. …

Cancer ResearchPathologymedicine.medical_specialtymicemedicine.drug_classMolecular Sequence DataGene ExpressionBiologyMonoclonal antibodyMalignant transformationAntigenmedicineProtein IsoformsAnimalsHumansNeoplasms Glandular and EpithelialMembrane Proteins/geneticsAntibodies Monoclonal/immunologyProtein Isoforms/immunologyBase SequenceReverse Transcriptase Polymerase Chain ReactionNeoplasms Glandular and Epithelial/drug therapyAntibodies MonoclonalImmunotherapy ActiveMembrane ProteinsCancermedicine.diseaseFlow CytometryImmunohistochemistryImmunotherapy Active/methodsOncologyCancer cellClaudinsbiology.proteinCancer researchImmunohistochemistryAntibodyStem cell
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Transforming Growth Factor-β–Mediated Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand Expression and Apoptosis in Hepatoma Cells Requires Fun…

2008

Abstract Transforming growth factor-β (TGF-β) has been shown to induce apoptotic cell death in normal and transformed hepatocytes. We recently identified tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) as an important mediator of TGF-β–induced apoptosis in hepatoma cells. In this study, we have further explored the mechanism by which TGF-β up-regulates TRAIL expression. The 5′-flanking region of the TRAIL gene was isolated and characterized. Deletion mutants of the 5′-untranslated region of the TRAIL gene revealed a region comprising nucleotides −1950 to −1100 responsible for TRAIL induction following treatment with TGF-β. Within this region, we have identified an activator …

Cancer ResearchProgrammed cell deathCarcinoma HepatocellularMolecular Sequence DataApoptosisSmad ProteinsSMADBiologyTNF-Related Apoptosis-Inducing LigandTransforming Growth Factor betaCell Line TumorHumansGene SilencingPromoter Regions GeneticMolecular BiologySmad4 ProteinBase SequenceActivator (genetics)Liver NeoplasmsDNA NeoplasmTranscription Factor AP-1OncologyCell cultureApoptosisMutationCancer researchTumor necrosis factor alphaProtein BindingSignal TransductionTransforming growth factorFOSBMolecular Cancer Research
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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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Transforming growth factor-β1, β2, and β3, urokinase and parathyroid hormone-related peptide expression in 8701-BC breast cancer cells and clones

1993

8701-BC is a recently characterized cell line isolated from a primary ductal infiltrating carcinoma of the breast (d.i.c.), showing some pleomorphism in cell microanatomy at an ultrastructural level. We have obtained different sublines of 8701-BC cells by cloning in soft agar at different concentrations (0.3% and 0.6%), and we have characterized the cloned lines by some morphological and growth parameters. 8701-BC cells and clones have been submitted to analysis by reverse transcriptase-linked polymerase chain reaction to detect mRNAs of various cytokines (transforming growth factor-beta s, tumour necrosis factors, interleukin 1s, interleukin 6, parathyroid hormone-related peptide, gamma in…

Cancer Researchmedicine.medical_specialtyMolecular Sequence DataParathyroid hormoneBreast NeoplasmsPolymerase Chain ReactionTransforming Growth Factor betaInternal medicineGene expressionBiomarkers TumorTumor Cells CulturedmedicineHumansRNA MessengerMolecular BiologyBase SequencebiologyParathyroid hormone-related proteinInterleukin-6Tumor Necrosis Factor-alphaCarcinoma Ductal BreastParathyroid Hormone-Related ProteinProteinsInterleukinCell BiologyTransforming growth factor betaUrokinase-Type Plasminogen ActivatorMolecular biologyIn vitroClone CellsPhenotypeEndocrinologyCell culturebiology.proteinInterleukin-1Developmental BiologyTransforming growth factorDifferentiation
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Physiological mechanisms regulating the expression of endothelial-type NO synthase

2002

Although endothelial nitric oxide synthase (eNOS) is a constitutively expressed enzyme, its expression is regulated by a number of biophysical, biochemical, and hormonal stimuli, both under physiological conditions and in pathology. This review summarizes the recent findings in this field. Shear stress, growth factors (such as transforming growth factor-beta, fibroblast growth factor, vascular endothelial growth factor, and platelet-derived growth factor), hormones (such as estrogens, insulin, angiotensin II, and endothelin 1), and other compounds (such as lysophosphatidylcholine) upregulate eNOS expression. On the other hand, the cytokine tumor necrosis factor-alpha and bacterial lipopolys…

Cancer Researchmedicine.medical_specialtyNitric Oxide Synthase Type IIIPhysiologyRNA Stabilitymedicine.medical_treatmentClinical BiochemistryBiologyFibroblast growth factorBiochemistryGene Expression Regulation Enzymologicchemistry.chemical_compoundEnosInternal medicinemedicineAnimalsPromoter Regions GeneticRegulation of gene expressionBase SequenceGene Expression ProfilingGrowth factorbiology.organism_classificationActin cytoskeletonAngiotensin IICell biologyVascular endothelial growth factorEndocrinologychemistryNitric Oxide SynthaseSignal transductionSignal TransductionNitric Oxide
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Role of the progesterone receptor for paclitaxel resistance in primary breast cancer

2007

Paclitaxel plays an important role in the treatment of primary breast cancer. However, a substantial proportion of patients treated with paclitaxel does not appear to derive any benefit from this therapy. We performed a prospective study using tumour cells isolated from 50 primary breast carcinomas. Sensitivity of primary tumour cells to paclitaxel was determined in a clinically relevant range of concentrations (0.85-27.2 microg ml(-1) paclitaxel) using an ATP assay. Chemosensitivity data were used to study a possible association with immunohistochemically determined oestrogen and progesterone receptor (ER and PR) status, as well as histopathological parameters. Progesterone receptor (PR) m…

Cancer Researchmedicine.medical_specialtyReceptor StatusPaclitaxelmedicine.medical_treatmentBreast Neoplasmsprogesterone receptorchemistry.chemical_compoundBreast cancerInternal medicineProgesterone receptormedicineHumansRNA Messengerprimary tumour cellsChemotherapyBase SequenceDose-Response Relationship Drugbusiness.industryAntineoplastic AgentsPhytogenic/therapeutic use/Base Sequence/Breast Neoplasms/Pathology/DNA Probes/Dose-Response RelationshipDrug/Drug ResistanceNeoplasm/Humans/Immunohistochemistry/Paclitaxel/RNAMessenger/genetics/ReceptorsProgesterone/physiologyindividualized chemotherapymedicine.diseaseAntineoplastic Agents PhytogenicImmunohistochemistryIn vitrochemosensitivityEndocrinologyOncologyPaclitaxelchemistryDrug Resistance NeoplasmCancer researchImmunohistochemistryTranslational TherapeuticsDNA ProbesReceptors ProgesteroneBreast carcinomabusinessBritish Journal of Cancer
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