Search results for "Telangiectasia"

showing 10 items of 32 documents

Artesunate induces oxidative DNA damage, sustained DNA double-strand breaks, and the ATM/ATR damage response in cancer cells.

2011

Abstract Artesunate, the active agent from Artemisia annua L. used in the traditional Chinese medicine, is being applied as a first-line drug for malaria treatment, and trials are ongoing that include this drug in cancer therapy. Despite increasing interest in its therapeutic application, the mode of cell killing provoked by artesunate in human cells is unknown. Here, we show that artesunate is a powerful inducer of oxidative DNA damage, giving rise to formamidopyrimidine DNA glycosylase–sensitive sites and the formation of 8-oxoguanine and 1,N6-ethenoadenine. Oxidative DNA damage was induced in LN-229 human glioblastoma cells dose dependently and was paralleled by cell death executed by ap…

Cancer ResearchProgrammed cell deathDNA RepairRAD51Drug Evaluation PreclinicalArtesunateApoptosisCell Cycle ProteinsAtaxia Telangiectasia Mutated ProteinsBiologyProtein Serine-Threonine KinasesModels Biologicalchemistry.chemical_compoundNeoplasmsTumor Cells CulturedHumansDNA Breaks Double-StrandedTumor Suppressor ProteinsMolecular biologyAntineoplastic Agents PhytogenicArtemisininsUp-RegulationNon-homologous end joiningDNA-Binding ProteinsOxidative StressCell killingOncologychemistryArtesunateApoptosisCancer cellHomologous recombinationDNA DamageMolecular cancer therapeutics
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ATRIP protects progenitor cells against DNA damage in vivo

2020

AbstractThe maintenance of genomic stability during the cell cycle of progenitor cells is essential for the faithful transmission of genetic information. Mutations in genes that ensure genome stability lead to human developmental syndromes. Mutations in Ataxia Telangiectasia and Rad3-related (ATR) or in ATR-interacting protein (ATRIP) lead to Seckel syndrome, which is characterized by developmental malformations and short life expectancy. While the roles of ATR in replicative stress response and chromosomal segregation are well established, it is unknown how ATRIP contributes to maintaining genomic stability in progenitor cells in vivo. Here, we generated the first mouse model to investigat…

CheckpointsProgrammed cell deathDNA damage[SDV]Life Sciences [q-bio]610 MedizinBiologyDNA replicationDNA damage responseArticle03 medical and health sciences0302 clinical medicine610 Medical sciencesmedicineProgenitor celllcsh:QH573-671GeneMitosisComputingMilieux_MISCELLANEOUSCell proliferation030304 developmental biology0303 health scienceslcsh:CytologyDisease modelCell cyclemedicine.diseaseCell biologyApoptosis030220 oncology & carcinogenesisAtaxia-telangiectasiaCell Death & Disease
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Apoptotic death induced by the cyclophosphamide analogue mafosfamide in human lymphoblastoid cells: Contribution of DNA replication, transcription in…

2007

Cyclophosphamide is one of the most often used anticancer drugs. Although DNA interstrand cross-links are considered responsible for its cytotoxicity, the mechanism of initiation and execution of cell death is largely unknown. Using the cyclophosphamide analogue mafosfamide, which does not need metabolic activation, we show that mafosfamide induces apoptosis dose and time dependently in lymphoblastoid cells, with clearly more apoptosis in p53(wt) cells. We identified two upstream processes that initiate apoptosis, DNA replication blockage and transcriptional inhibition. In lymphoblastoid cells, wherein DNA replication can be switched off by tetracycline, proliferation is required for induci…

DNA ReplicationProgrammed cell deathTime FactorsTranscription GeneticDNA damageDrug ResistanceAntineoplastic AgentsApoptosisCell Cycle ProteinsAtaxia Telangiectasia Mutated ProteinsProtein Serine-Threonine KinasesToxicologyCaspase-Dependent ApoptosisCell Linechemistry.chemical_compoundMafosfamideHumansCHEK1PhosphorylationCyclophosphamideCaspaseCell ProliferationPharmacologyDose-Response Relationship DrugbiologyTumor Suppressor ProteinsCell cycleDNA-Binding ProteinsCheckpoint Kinase 2chemistryApoptosisCaspasesCheckpoint Kinase 1Cancer researchbiology.proteinTumor Suppressor Protein p53Protein KinasesSignal TransductionToxicology and Applied Pharmacology
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Class 1 Histone Deacetylases and Ataxia-Telangiectasia Mutated Kinase Control the Survival of Murine Pancreatic Cancer Cells upon dNTP Depletion

2021

Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive disease with a dismal prognosis. Here, we show how an inhibition of de novo dNTP synthesis by the ribonucleotide reductase (RNR) inhibitor hydroxyurea and an inhibition of epigenetic modifiers of the histone deacetylase (HDAC) family affect short-term cultured primary murine PDAC cells. We used clinically relevant doses of hydroxyurea and the class 1 HDAC inhibitor entinostat. We analyzed the cells by flow cytometry and immunoblot. Regarding the induction of apoptosis and DNA replication stress, hydroxyurea and the novel RNR inhibitor COH29 are superior to the topoisomerase-1 inhibitor irinotecan which is used to treat PDAC. Ent…

DNA Replicationendocrine system diseasesDNA damagereplication stressQH301-705.5RNR Inhibitor COH29Antineoplastic AgentsCell Cycle ProteinsRNRAtaxia Telangiectasia Mutated ProteinsArticle03 medical and health scienceschemistry.chemical_compoundAtaxia TelangiectasiaMice0302 clinical medicineHDACAnimalscancerPDAC cellsRibonucleotide Reductase SubunitEnzyme InhibitorsBiology (General)030304 developmental biology0303 health sciencesbiologyChemistryEntinostatDNA replicationapoptosisGeneral Medicine3. Good healthPancreatic NeoplasmsHistoneRibonucleotide reductase030220 oncology & carcinogenesisATMbiology.proteinCancer researchDNA damageHistone deacetylaseCells
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High resistance to X-rays and therapeutic carbon ions in glioblastoma cells bearing dysfunctional ATM associates with intrinsic chromosomal instabili…

2014

To investigate chromosomal instability and radiation response mechanisms in glioblastoma cells.We undertook a comparative analysis of two patient-derived glioblastoma cell lines. Their resistance to low and high linear energy transfer (LET) radiation was assessed using clonogenic survival assay and their intrinsic chromosome instability status using fluorescence in situ hybridization. DNA damage was analyzed by pulsed-field gel electrophoresis and by γ-H2AX foci quantification. Expression of DNA damage response proteins was assessed by immunoblot.Increased radioresistance to X-rays as well as carbon ions was observed in glioblastoma cells exhibiting high levels of naturally occurring chromo…

Genome instabilityDNA RepairDNA damageLinear energy transferHeavy Ion RadiotherapyAtaxia Telangiectasia Mutated ProteinsBiologyRadiation ToleranceCell Line TumorChromosomal InstabilityRadioresistanceChromosome instabilitymedicineHumansDNA Breaks Double-StrandedLinear Energy TransferRadiology Nuclear Medicine and imagingGel electrophoresisRadiological and Ultrasound Technologymedicine.diagnostic_testX-RaysCell CycleGenomicsMolecular biologyPhosphorylationGlioblastomaSignal TransductionFluorescence in situ hybridizationInternational Journal of Radiation Biology
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Study of the cytolethal distending toxin (CDT)-activated cell cycle checkpoint. Involvement of the CHK2 kinase.

2001

AbstractThe bacterial cytolethal distending toxin (CDT) triggers a G2/M cell cycle arrest in eukaryotic cells by inhibiting the CDC25C phosphatase-dependent CDK1 dephosphorylation and activation. We report that upon CDT treatment CDC25C is fully sequestered in the cytoplasmic compartment, an effect that is reminiscent of DNA damage-dependent checkpoint activation. We show that the checkpoint kinase CHK2, an upstream regulator of CDC25C, is phosphorylated and activated after CDT treatment. In contrast to what is observed with other DNA damaging agents, we demonstrate that the activation of CHK2 can only take place during S-phase. Use of wortmannin and caffeine suggests that this effect is no…

Intracellular FluidCell cycle checkpointCytolethal distending toxinCell Cycle ProteinsAtaxia Telangiectasia Mutated ProteinsBiochemistryS PhaseWortmanninchemistry.chemical_compoundStructural BiologyPhosphorylation0303 health sciences030302 biochemistry & molecular biologyCell CycleCell cycleProtein-Tyrosine Kinases3. Good healthCell biologyDNA-Binding Proteinsbiological phenomena cell phenomena and immunityWortmanninG2 PhaseCytolethal distending toxinBacterial ToxinsProto-Oncogene Proteins pp60(c-src)Biophysics[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologyProtein Serine-Threonine KinasesCell Line03 medical and health sciencesCaffeineGeneticsHumanscdc25 PhosphatasesCHEK1Molecular Biology[SDV.BC] Life Sciences [q-bio]/Cellular Biology030304 developmental biologyCheckpoint 2 kinaseCyclin-dependent kinase 1Cell growthTumor Suppressor ProteinsCell BiologyG2-M DNA damage checkpointCDC25CAndrostadienesGenes cdcchemistryCancer researchHeLa CellsFEBS letters
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Deletion of 11q in Neuroblastomas Drives Sensitivity to PARP Inhibition

2017

AbstractPurpose: Despite advances in multimodal therapy, neuroblastomas with hemizygous deletion in chromosome 11q (20%–30%) undergo consecutive recurrences with poor outcome. We hypothesized that patients with 11q-loss may share a druggable molecular target(s) that can be exploited for a precision medicine strategy to improve treatment outcome.Experimental Design: SNP arrays were combined with next-generation sequencing (NGS) to precisely define the deleted region in 17 primary 11q-loss neuroblastomas and identify allelic variants in genes relevant for neuroblastoma etiology. We assessed PARP inhibitor olaparib in combination with other chemotherapy medications using both in vitro and in v…

Male0301 basic medicineCancer ResearchDNA repairAntineoplastic AgentsAtaxia Telangiectasia Mutated ProteinsKaplan-Meier EstimatePoly(ADP-ribose) Polymerase InhibitorsBiologyModels BiologicalPolymorphism Single NucleotideImmunophenotypingOlaparibNeuroblastoma03 medical and health scienceschemistry.chemical_compound0302 clinical medicineRecurrenceCell Line TumorNeuroblastomaBiomarkers TumormedicineAnimalsHumansAllelesNeoplasm StagingCisplatinTemozolomideChromosomes Human Pair 11High-Throughput Nucleotide SequencingCancerDrug SynergismPrognosismedicine.diseaseXenograft Model Antitumor AssaysMolecular biologyDisease Models Animal030104 developmental biologyOncologychemistryDrug Resistance Neoplasm030220 oncology & carcinogenesisPARP inhibitorCancer researchFemaleChromosome DeletionHaploinsufficiencyBiomarkersmedicine.drugClinical Cancer Research
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Immunological investigations in two brothers with ataxia telangiectasia Louis-Bar

1976

Two of three brothers with the classical signs of ataxia telangiectasia were investigated for their immunological disorders at the ages of 13 and 16 years, respectively. The elder brother also suffers from autoimmune hemolytic anemia, a complication which has not yet been described in the course of ataxia telangiectasia. Immunological investigations made in both brothers showed a reduction in the number and function of T lymphocytes. The number of B lymphocytes was normal, among which there were cells staining for IgA, although serum IgA was absent. It seems possible that this phenomenon is caused by a disturbance in the process of maturation of lymphoid cells with a lack of differentiation…

MaleB-Lymphocytescongenital hereditary and neonatal diseases and abnormalitiesAdolescentbusiness.industryT-LymphocytesPlasma CellsGeneral MedicineSerum igamedicine.diseaseImmunoglobulin AAtaxia TelangiectasiaIMMUNE DEFICIENCY DISEASEPediatrics Perinatology and Child HealthImmunologyAtaxia-telangiectasiamedicineHumansRadiology Nuclear Medicine and imagingAnemia Hemolytic AutoimmuneAutoimmune hemolytic anemiaComplicationbusinessEuropean Journal of Pediatrics
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Health‐Related Quality of Life in Hereditary Hemorrhagic Telangiectasia

2007

Objective To assess and differentiate the health-related quality of life (HR-QoL) in patients with hereditary hemorrhagic telangiectasia (HHT). Study Design and Setting A prospective, open, cross-sectional questionnaire-based study (including the Short Form-36 Health Survey [SF-36]) performed by a tertiary care center. Results A total of 77 patients (36 females) were included. Except for one domain (bodily pain), the scores for all scales of the SF-36 were significantly reduced in comparison with normative data. The duration of epistaxis, the presence of hepatic involvement and gastrointestinal bleeding, and the number of visible telangiectases correlated with lower scores on several scales…

MaleGastrointestinal bleedingmedicine.medical_specialtyPediatricsCross-sectional studyHealth StatusMEDLINETelangiectases03 medical and health sciences0302 clinical medicineQuality of lifeRecurrenceSurveys and QuestionnairesmedicineHumansProspective Studies030223 otorhinolaryngologyProspective cohort studyTelangiectasiaHealth related quality of lifebusiness.industrymedicine.diseaseCross-Sectional StudiesOtorhinolaryngology030220 oncology & carcinogenesisQuality of LifePhysical therapyFemaleTelangiectasia Hereditary HemorrhagicSurgerymedicine.symptombusinessOtolaryngology–Head and Neck Surgery
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Cancer in Children With Fanconi Anemia and Ataxia-Telangiectasia—A Nationwide Register-Based Cohort Study in Germany

2021

PURPOSE Fanconi anemia (FA) and ataxia-telangiectasia (AT) are rare inherited syndromes characterized by abnormal DNA damage response and caused by pathogenic variants in key DNA repair proteins that are also relevant in the pathogenesis of breast cancer and other cancer types. The risk of cancer in children with these diseases is poorly understood and has never been assessed in a population-based cohort before. METHODS We identified 421 patients with FA and 160 patients with AT diagnosed between 1973 and 2020 through German DNA repair disorder reference laboratories. We linked patients' laboratory data with childhood cancer data from the German Childhood Cancer Registry. RESULTS Among 421 …

MaleOncologyRegister basedCancer Researchmedicine.medical_specialtyTime FactorsAdolescentDNA damageAnemiaDNA repairRisk AssessmentAtaxia TelangiectasiaRisk FactorsFanconi anemiaGermanyNeoplasmsInternal medicinemedicineHumansRegistriesChildbusiness.industryIncidenceAge FactorsInfantCancerPrognosismedicine.diseaseFanconi AnemiaOncologyChild PreschoolAtaxia-telangiectasiaFemalebusinessCohort studyJournal of Clinical Oncology
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