Search results for "Etoposide"

showing 10 items of 97 documents

Langerhans's cell histiocytosis in old subjects: two rare case reports and review of the literature

2012

Background: Langerhans cell histiocytosis (LCH) is a proliferative disease of histiocyte-like cells that generally affects children; LCH onset is rare in adults; immunohistochemistry is essential to obtain the correct diagnosis, and treatment protocols are controversial. Objective: To describe two new cases of adult onset oral LCH. Case reports: Case 1: a 71-year-old woman, complaining of diffuse oral pain, presented with erythematous mucosal lesions; the panoramic radiograph and CT scan showed multiple mandible radiolucent areas. Immunohistochemical assay for S-100, CD1a and langerin test was essential in reaching the correct diagnosis. Case 2: a 77-year-old female patient presented with a…

PalateLangerhans's cell histiocytosisS100 ProteinsAntineoplastic AgentsAntineoplastic Agents Phytogeniclangerhans’s cell histiocytosis old subjects langerin oral immunohistochemistryAntigens CD1Diagnosis DifferentialSettore MED/28 - MALATTIE ODONTOSTOMATOLOGICHEHistiocytosis Langerhans-CellMannose-Binding LectinsAntigens CDErythemaCladribineHumansFemaleLectins C-TypeMandibular DiseasesRadiotherapy AdjuvantVulvar DiseasesMouth DiseasesPeriodontal DiseasesAgedEtoposide
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Development and Partial Characterization of a Human T-Lymphoblastic Leukemic (CCRF-CEM) Cell Line Resistant to Etoposide. Analysis of Possible Circum…

1996

We have selected an etoposide-resistant variant (CCRF-CEM/VP-16) of the human T-lymphoblastic CCRF-CEM leukemia for study. Resistance to the topoisomerase II (topo II) inhibitor was about 11-fold and stable. Other data revealed that the new cell line had acquired an atypical, non-P-glycoprotein overexpressing multidrug resistant (MDR) phenotype with cross-resistance to other topo II inhibitors (amsacrine, doxorubicin, and mitoxantrone) and to glucocorticoids, but not to novobiocin, ICRF-187, vincristine or cisplatin. In a first instance, we assumed that altered drug-topo II interactions, based on quantitative and/or qualitative modifications of the enzyme, are a cause of resistance in the c…

PharmacologyMitoxantroneVincristineLeukemia T-CellDrug resistanceBiologymedicine.diseaseAntineoplastic Agents PhytogenicDrug Resistance MultipleMultiple drug resistanceLeukemiaInfectious DiseasesOncologyDrug Resistance NeoplasmCyclosporin aImmunologyTumor Cells CulturedmedicineCancer researchHumansPharmacology (medical)AmsacrineEtoposideEtoposidemedicine.drugJournal of Chemotherapy
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Macrophage-mediated clearance of cells undergoing caspase-3-independent death

2003

Little is known of the functions of caspases in mediating the surface changes required for phagocytosis of dying cells. Here we investigate the role played by the effector caspase, caspase-3 in this process using the caspase-3-defective MCF-7 breast carcinoma line and derived caspase-3-expressing transfectants. Our results indicate that, while certain typical features of apoptosis induced by etoposide - namely classical morphological changes and the ability to degrade DNA into oligonucleosomal fragments - are caspase-3-dependent, loss of cell adhesion to plastic and the capacity to interact with, and to be phagocytosed by, human monocyte-derived macrophages - both by CD14-dependent and CD14…

Programmed cell deathTime FactorsBlotting WesternGreen Fluorescent ProteinsLipopolysaccharide ReceptorsApoptosisCaspase 3PhosphatidylserinesDNA FragmentationTransfectionCaspase 7Proinflammatory cytokinePhagocytosisCell Line TumorSettore BIO/10 - BiochimicaHumansMacrophageAnnexin A5Cell adhesionCytokineMolecular BiologyCells CulturedCaspaseEtoposideCaspase 7InflammationCell DeathbiologyCaspase 3MacrophagesDNACell BiologyCaspaseCell biologyEnzyme ActivationLuminescent ProteinsApoptosisCaspasesbiology.proteinCytokinesElectrophoresis Polyacrylamide GelCell Death & Differentiation
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Synchronous Two Distinct Neuroendocrine Lung Cancer Lesions

2015

Synchroniczne nowotwory płuc są rzadką chorobą, a prezentowany przypadek to pierwszy opublikowany opis jednoczesnego wystąpienia dwóch pierwotnych neuroendokrynnych raków płuca zlokalizowanych w jednym płacie. Przedstawiono przypadek 55-letniej pacjentki z dwoma pierwotnymi, odrębnymi neuroendokrynnymi rakami płata górnego płuca prawego. Pacjentka została przyjęta na oddział chirurgii klatki piersiowej w celu diagnostyki dwóch cieni okrągłych płuca prawego (o średnicy 11 i 19 mm) uwidocznionych na zdjęciu RTG klatki piersiowej wykonanym trzy miesiące wcześniej. Przy przyjęciu pacjentka nie prezentowała żadnych objawów związanych ze zmianami w płucu. Dalsze badania obrazowe wykazały zmiennoś…

Pulmonary and Respiratory MedicinePathologymedicine.medical_specialtyLung NeoplasmsLung biopsySmall-cell carcinomasynchronous primary lung cancerNeoplasms Multiple PrimarymedicineHumansCarcinoma Small CellLung cancerdrobnokomórkowy rak płucalarge cell neuroendocrine carcinomasmall cell carcinomaEtoposideCisplatinLungbusiness.industrywielkokomórkowy neuroendokrynny rak płucaNeoplasms Second PrimaryMiddle Agedmedicine.diseaseCarcinoma Neuroendocrinemedicine.anatomical_structureCardiothoracic surgeryFemaleProphylactic cranial irradiationTomography X-Ray Computedbusinesssynchroniczny rak płucamedicine.drugAdvances in Respiratory Medicine
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DNA damage causes TP53-dependent coupling of self-renewal and senescence pathways in embryonal carcinoma cells.

2013

Recent studies have highlighted an apparently paradoxical link between self-renewal and senescence triggered by DNA damage in certain cell types. In addition, the finding that TP53 can suppress senescence has caused a re-evaluation of its functional role in regulating these outcomes. To investigate these phenomena and their relationship to pluripotency and senescence, we examined the response of the TP53-competent embryonal carcinoma (EC) cell line PA-1 to etoposide-induced DNA damage. Nuclear POU5F1/OCT4A and P21CIP1 were upregulated in the same cells following etoposide-induced G 2M arrest. However, while accumulating in the karyosol, the amount of OCT4A was reduced in the chromatin fract…

SenescenceCyclin-Dependent Kinase Inhibitor p21OCT4A/POU5F1Embryonal Carcinoma Stem CellssenescenceDNA RepairDNA repairDNA damagetumor cellsBiologyProtein Serine-Threonine Kinasesself-renewalHistonesAurora KinasesCell Line TumorReportAutophagyAurora Kinase BHumansTP53PhosphorylationRNA Small InterferingMolecular BiologyMitosisCellular SenescenceCyclin-Dependent Kinase Inhibitor p16EtoposideOvarian NeoplasmsEmbryonal Carcinoma Stem CellsCell BiologyG2-M DNA damage checkpointbeta-GalactosidasepluripotencyAntineoplastic Agents PhytogenicChromatinUp-RegulationG2 Phase Cell Cycle CheckpointsCheckpoint Kinase 2Cancer researchDNA damageFemaleRNA InterferenceRad51 RecombinaseTumor Suppressor Protein p53Cell agingOctamer Transcription Factor-3Developmental BiologyCell cycle (Georgetown, Tex.)
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Acrylamide catalytically inhibits topoisomerase II in V79 cells.

2010

The vinyl monomer acrylamide is characterized by the presence of an alpha,beta-unsaturated carbonyl group that makes it reactive towards thiol, hydroxyl or amino groups and towards the nucleophilic centers in DNA. The ability of acrylamide to chemically modify protein thiols has prompted us to consider topoisomerase II as one possible target of acrylamide, since agents targeting protein sulfhydryl groups act as either catalytic inhibitors or poisons of topoisomerase II. Nuclear extracts from V79 Chinese hamster cells incubated with acrylamide reduced topoisomerase II activity as inferred by an inability to convert kinetoplast DNA to the decatenated form. Nuclear extracts incubated with acry…

ToxicologyCleavage (embryo)Cell LineColony-Forming Units AssayV79 cellchemistry.chemical_compoundCell Line TumorCricetinaemedicineAnimalsTopoisomerase II InhibitorsDNA CleavageEtoposideEtoposideNucleic Acid Synthesis Inhibitorschemistry.chemical_classificationCell NucleusAcrylamidebiologyTopoisomeraseDNA KinetoplastGeneral MedicineTopoisomerase IIAntineoplastic Agents PhytogenicSettore BIO/18 - GeneticaEnzymechemistryBiochemistryKinetoplastAcrylamidebiology.proteinTopoisomerase-II InhibitorDNAmedicine.drugToxicology in vitro : an international journal published in association with BIBRA
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ChemInform Abstract: Synthesis and Induction of G0-G1 Phase Arrest with Apoptosis of 3,5-Dimethyl-6-phenyl-8-(trifluoromethyl)-5,6-dihydropyrazolo[3,…

2009

The multistep synthesis of 3,5-dimethyl-6-phenyl-8-(trifluoromethyl)-5,6-dihydropyrazolo[3,4-f][1,2,3,5]tetrazepin-4(3H)-one 15 has been carried out. The compound showed antiproliferative and apoptotic effects against K562, K562-R (imatinib mesilate resistant), HL60 and multidrug resistant (MDR) HL60 cell lines. Compound 15 showed a pro-apoptotic activity against HL60 and K562 resistant cell lines markedly higher than etoposide and busulfan, respectively. Flow cytometry studies carried out on K562 cells allowed to establish that 15 induces G0-G1 phase arrest followed by apoptosis.

Trifluoromethylmedicine.diagnostic_testHL60General MedicineMolecular biologyFlow cytometryMultiple drug resistancechemistry.chemical_compoundchemistryApoptosishemic and lymphatic diseasesmedicineBusulfanEtoposidemedicine.drugK562 cellsChemInform
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Clinical aspects and prognosis of ependymoma in infants and children

2001

Thirty-two patients (22 boys and 10 girls) with a histologically confirmed diagnosis of ependymoma were treated between 1972 and 1999. A total macroscopic resection was achieved in 16 of these patients, whereas 15 resections were classified by the surgeon as subtotal. In 1 patient a ventriculostomy was created as part of a palliative strategy. All children over 3 years old were treated with postoperative radiotherapy. Chemotherapy consisted of procarbazine, ifosfamide, etoposide, methotrexate, cisplatin and cytosine arabinoside. There was 1 perioperative death. Twenty children developed a relapse of disease within 2 months to 13 years and 1 month after the initial therapy. A maximal number …

VentriculostomyEpendymomamedicine.medical_specialtyChemotherapyIfosfamidebusiness.industrymedicine.medical_treatmentGeneral MedicineProcarbazinemedicine.diseaseSurgeryEl NiñoPediatrics Perinatology and Child HealthmedicineNeurology (clinical)NeurosurgerybusinessEtoposidemedicine.drugChild's Nervous System
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Drivers of topoisomerase II poisoning mimic and complement cytotoxicity in AML cells

2019

Recently approved cancer drugs remain out-of-reach to most patients due to prohibitive costs and only few produce clinically meaningful benefits. An untapped alternative is to enhance the efficacy and safety of existing cancer drugs. We hypothesized that the response to topoisomerase II poisons, a very successful group of cancer drugs, can be improved by considering treatment-associated transcript levels. To this end, we analyzed transcriptomes from Acute Myeloid Leukemia (AML) cell lines treated with the topoisomerase II poison etoposide. Using complementary criteria of co-regulation within networks and of essentiality for cell survival, we identified and functionally confirmed 11 druggabl…

biologyCombination therapybusiness.industryTopoisomeraseMyeloid leukemiatopoisomerase II poisonscombination therapyCell killingOncologygene expressioncancer essentialitybiology.proteinmedicineCancer researchDNA damageCytotoxic T cellCytotoxicitybusinessEtoposidePI3K/AKT/mTOR pathwayResearch Papermedicine.drugOncotarget
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WRN protects against topo I but not topo II inhibitors by preventing DNA break formation

2008

The Werner syndrome helicase/3′-exonuclease (WRN) is a major component of the DNA repair and replication machinery. To analyze whether WRN is involved in the repair of topoisomerase-induced DNA damage we utilized U2-OS cells, in which WRN is stably down-regulated (wrn-kd), and the corresponding wild-type cells (wrn-wt). We show that cells not expressing WRN are hypersensitive to the toxic effect of the topoisomerase I inhibitor topotecan, but not to the topoisomerase II inhibitor etoposide. This was shown by mass survival assays, colony formation and induction of apoptosis. Upon topotecan treatment WRN deficient cells showed enhanced DNA replication inhibition and S-phase arrest, whereas af…

congenital hereditary and neonatal diseases and abnormalitiesWerner Syndrome HelicaseDNA RepairCell SurvivalDNA damageDNA repairBlotting WesternApoptosisBone NeoplasmsBiologyTopoisomerase-I InhibitorBiochemistryArticleWerner Syndrome HelicaseColony-Forming Units AssayHistonesTumor Cells CulturedmedicineHumansTopoisomerase II InhibitorsEnzyme InhibitorsRNA Small InterferingeducationMolecular BiologyEtoposideOsteosarcomaeducation.field_of_studyRecQ HelicasesTopoisomeraseCell CycleDNA Breaksnutritional and metabolic diseasesCell BiologyAntineoplastic Agents PhytogenicMolecular biologyDNA Topoisomerases Type IIExodeoxyribonucleasesBromodeoxyuridineDNA Topoisomerases Type IDNA Replication InhibitionCancer researchbiology.proteinTopoisomerase I InhibitorsTopoisomerase-II InhibitorTopotecanCamptothecinmedicine.drugDNA Repair
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