Search results for "pyrimidine"

showing 10 items of 589 documents

Wavelength dependence of oxidative DNA damage induced by UV and visible light.

1997

DNA damage induced by UV radiation and visible light (290-500 nm) in AS52 Chinese hamster cells was analysed by an alkaline elution assay with specific repair endonucleases. Cells were exposed to extensively filtered monochrome or broad-band radiation. Between 290 and 315 nm, the ratio of base modifications sensitive to Fpg protein (i.e. 8-hydroxyguanine and formamidopyrimidines) and T4 endonuclease V (i.e. cyclobutane pyrimidine dimers) was constant (approximately 1:200), indicating that the direct excitation of DNA is responsible for both types of damage in this range of the spectrum. While the yield of pyrimidine dimers per unit dose continued to decrease exponentially beyond 315 nm, the…

Cancer ResearchPyrimidinebiologyLightSinglet oxygenDNA damageUltraviolet RaysPyrimidine dimerDose-Response Relationship RadiationGeneral MedicineCHO CellsPhotochemistrymedicine.disease_causechemistry.chemical_compoundEndonucleaseOxidative StresschemistryCricetinaebiology.proteinmedicineAnimalsDNAOxidative stressVisible spectrumDNA DamageCarcinogenesis
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Overexpression of Ogg1 in mammalian cells: effects on induced and spontaneous oxidative DNA damage and mutagenesis

1999

Chinese hamster ovary cell lines (AA8 and AS52) were stably transfected to overexpress hOgg1 protein, the human DNA repair glycosylase for 7,8-dihydro-8-oxoguanine (8-oxoG). In the transfectants, the repair rate of 8-oxoG residues induced by either potassium bromate or the photosensitizer [R]-1-[(10-chloro-4-oxo-3-phenyl-4H-benzo[a]quinolizin-1-yl)-carbo nyl ]-2-pyrrolidinemethanolplus light was up to 3-fold more rapid than in the parental cells. However, the improved repair had little effect on the mutagenicity of potassium bromate in the guanine phosphoribosyl transferase (gpt) locus of the OGG1-transfected AS52 cells. The steady-state (background) levels of DNA base modifications sensiti…

Cancer ResearchPyrrolidinesDNA RepairPhotochemistryDNA repairDNA damageBiologyTransfectionPolymerase Chain ReactionCell LineDNA-formamidopyrimidine glycosylasechemistry.chemical_compoundCricetulusGenes ReporterCricetinaeAnimalsheterocyclic compoundsN-Glycosyl HydrolasesPhotosensitizing AgentsBromatesChinese hamster ovary cellOvaryGeneral MedicineTransfectionDNA repair protein XRCC4OxidantsMolecular biologyOxidative StressDNA-Formamidopyrimidine GlycosylasechemistryGenes BacterialMutagenesisDNA glycosylaseEnzyme InductionFemaleQuinolizinesDNADNA DamageCarcinogenesis
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Galangin increases the cytotoxic activity of imatinib mesylate in imatinib-sensitive and imatinib-resistant Bcr-Abl expressing leukemia cells

2008

Resistance to imatinib mesylate is an emergent problem in the treatment of Bcr-Abl expressing myelogenous leukemias and additional therapeutic strategies are required. We observed that galangin, a non-toxic, naturally occurring flavonoid was effective as anti-proliferative, and apoptotic agent in Bcr-Abl expressing K562 and KCL22 cells and in imatinib mesylate resistant K562-R and KCL22-R cells. Galangin induced an arrest of cells in G0–G1phase of cell cycle and a decrease in pRb, cdk4, cdk1, cycline B levels; moreover, it was able to induce a monocytic differentiation of leukemic Bcr-Abl+ cells. Of note, galangin caused a decrease in Bcl-2 levels and markedly increased the apoptotic activi…

Cancer ResearchSettore MED/17 - Malattie InfettiveSettore MED/06 - Oncologia MedicaApoptosisPharmacologyResting Phase Cell CyclePiperazineschemistry.chemical_compoundCell Line TumorLeukemia Myelogenous Chronic BCR-ABL Positivehemic and lymphatic diseasesAntineoplastic Combined Chemotherapy ProtocolsmedicineHumansCytotoxic T cellChrysinneoplasmsFlavonoidsLeukemiaG1 PhaseApoptosiCell DifferentiationImatinibmedicine.diseaseSettore CHIM/08 - Chimica FarmaceuticaGalanginLeukemiaPyrimidinesImatinib mesylateOncologychemistryDrug Resistance NeoplasmImatinibBenzamidesSettore BIO/14 - FarmacologiaImatinib MesylateK562 CellsFisetinBcr-AblK562 cellsmedicine.drugCancer Letters
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Carboxyamidotriazole inhibits cell growth of imatinib-resistant chronic myeloid leukaemia cells including T315I Bcr-Abl mutant by a redox-mediated me…

2010

Mutation of the Bcr–Abl oncoprotein is one of most frequent mechanisms by which chronic myelogenous leukemia (CML) cells become resistant to imatinib. Here, we show that treat- ment of cell lines harbouring wild type or mutant BCR–ABL with carboxyamidotriazole (CAI), a calcium influx and signal transduction inhibitor, inhibits cell growth, the expres- sion of Bcr–Abl and its downstream signalling, and induces apoptosis. Moreover, we show that CAI acts by increasing intracellular ROS. Clinically significant, CAI has also inhibitory effects on T315I Bcr–Abl mutant, a mutation that causes CML cells to become insensitive to imatinib and second generation abl kinase inhibitors.

Cancer Researchbcr-abl Carboxyamidotriazole chronic myeloid leukemia cells imatinibBlotting WesternFusion Proteins bcr-ablAntineoplastic AgentsApoptosisSignal transduction inhibitorBiologyPiperazineschemistry.chemical_compoundMicehemic and lymphatic diseasesCell Line TumorLeukemia Myelogenous Chronic BCR-ABL PositivemedicineAnimalsHumansneoplasmsCell ProliferationSettore MED/04 - Patologia GeneraleABLCarboxyamidotriazoleCell growthWild typeImatinibTriazolesmedicine.diseaseImatinib mesylatePyrimidinesOncologychemistryDrug Resistance NeoplasmBenzamidesMutationCancer researchImatinib MesylateReactive Oxygen SpeciesOxidation-ReductionChronic myelogenous leukemiamedicine.drug
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Adherence to ruxolitinib, an oral JAK1/2 inhibitor, in patients with myelofibrosis: interim analysis from an Italian, prospective cohort study (ROMEI…

2021

ROMEI, a prospective, observational study in patients with myelofibrosis receiving the oral JAK1/2 inhibitor ruxolitinib in real-world practice, assesses treatment adherence based on the 8-item Morisky Medication Adherence Scale (MMAS-8). Here, we present MMAS-8 results at week 24. Overall, 101 of 188 evaluable patients completed the questionnaire at every visit (full completers). Mean (±standard deviation) total MMAS-8 scores remained stable from week 4 to week 24 in the overall population (7.54 ± 0.77 and 7.67 ± 0.70, respectively) and full completers (7.53 ± 0.79 and 7.67 ± 0.73, respectively). Rates of low (MMAS-8 ˂6) or medium (MMAS-8 ≥ 6 to ˂8) adherence were 25–40% and 26–36%, respec…

Cancer Researchmedicine.medical_specialtyRuxolitinib8-item Morisky Medication Adherence ScalePsychometricsTreatment adherenceruxolitiniboral therapiesMedication AdherenceCohort StudiesTreatment complianceInternal medicineSurveys and QuestionnairesNitrilesmedicineHumansIn patientProspective StudiesProspective cohort studyMyelofibrosistreatment compliance8-item Morisky Medication Adherence Scale oral therapies ruxolitinib treatment compliance Adherencebusiness.industryHematologyJanus Kinase 1Janus Kinase 2Interim analysismedicine.disease8-item Morisky Medication Adherence Scale; Adherence; oral therapies; ruxolitinib; treatment compliancePyrimidinesOncologyAdherencePrimary MyelofibrosisPyrazolesObservational studybusinessmedicine.drugLeukemialymphoma
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A French prospective pilot study for identifying dihydropyrimidine dehydrogenase (DPD) deficiency in breast cancer patients (pts) receiving capecitab…

2013

e13519 Background: For fluoropyrimidines, and especially cap, Health Authorities point out that DPD deficiency confers a significant risk of major toxicity (tox). Identification of at-risk pts is thus relevant. This multicentric prospective study of the French GPCO group (Groupe de Pharmacologie Clinique Oncologique, Unicancer) evaluated the sensitivity, specificity and predictive values of DPD phenotyping and genotyping for predicting severe cap-related tox in metastatic breast cancer pts. Methods: 303 pts were included (15 institutions), 88% received cap as monotherapy, 28% were treated as first line (mean dose at 1st cycle 1957 mg/m2/d). Pre-treatment dihydrouracil (UH2) and uracil (U) …

Cancer Researchmedicine.medical_specialtymacromolecular substances030226 pharmacology & pharmacyGastroenterology[SPI.AUTO]Engineering Sciences [physics]/AutomaticCapecitabine03 medical and health scienceschemistry.chemical_compound0302 clinical medicineBreast cancerInternal medicine[ SPI.AUTO ] Engineering Sciences [physics]/AutomaticmedicineDihydropyrimidine dehydrogenaseProspective cohort studybusiness.industryDihydrouracilmedicine.diseaseMetastatic breast cancer3. Good healthSurgery[SPI.AUTO] Engineering Sciences [physics]/AutomaticOncologychemistry030220 oncology & carcinogenesisRelative riskToxicitybacteriaPublished in Journal of Clinical Oncology vol. 31 : 2013 (Suppl ;abstr e13519)businessmedicine.drug
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Key Enzymes in Pyrimidine Synthesis, CAD and CPS1, Predict Prognosis in Hepatocellular Carcinoma

2021

Simple Summary Individual patients with liver cancer have a highly variable clinical course. Hence, there is an urgent need to identify new prognostic markers to determine prognosis and select specific therapies. Expression of two key enzymes in pyrimidine synthesis was analyzed in a large, well-characterized cohort of patients with liver cancer. Dysregulated expression of these enzymes was associated with shorter survival of the patients. A combined score of both markers was found to be a statistically independent prognostic marker. Abstract Patients with hepatocellular carcinoma (HCC) have a highly variable clinical course. Therefore, there is an urgent need to identify new prognostic mar…

Cancer ResearchpyrimidineCADlcsh:RC254-282Article03 medical and health sciences0302 clinical medicinecps1medicineHCCchemistry.chemical_classificationTissue microarraybusiness.industryCancerhepatocellular carcinomaHCCSmedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensurea cycle dysregulationEnzymeDihydroorotasechemistryOncology030220 oncology & carcinogenesisHepatocellular carcinomaPyrimidine metabolismKey (cryptography)Cancer researchImmunohistochemistryBiomarker (medicine)biomarkercad030211 gastroenterology & hepatologyprognosisbusinessCancers
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Antibody generation and immunoassay development in diverse formats for pyrimethanil specific and sensitive analysis

2012

Immunochemical techniques are complementary tools to modern analytical requirements. These methods rely on the production of immunoreagents with adequate binding properties. In the present study, a rationally designed and functionalized derivative of pyrimethanil-a modern anilinopyrimidine fungicide-was synthesized in order to generate for the first time high-affinity and selective antibodies to this xenobiotic. A single coupling procedure-based on hapten activation using N,N′-disuccinimidyl carbonate and purification of the active ester-was followed to prepare both immunizing and assay conjugates. Polyclonal antibodies were produced and characterized by enzyme-linked immunosorbent assay (E…

Carrot juicePyrimethanilEnzyme-Linked Immunosorbent AssayBiochemistryAntibodiesAnalytical ChemistryBeverageschemistry.chemical_compoundLimit of DetectionElectrochemistrymedicineAnimalsEnvironmental ChemistrySpectroscopyFungicidesDetection limitImmunoassayResidue (complex analysis)Chromatographybiologymedicine.diagnostic_testChemistryDaucus carotaFungicides IndustrialPyrimidinesPolyclonal antibodiesImmunoassayAntibody Formationbiology.proteinFemalePyrimethanilELISARabbitsAntibodyHaptenHaptens
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Recent advances in the development of cyclin-dependent kinase 7 inhibitors.

2019

Abstract Cyclin dependent kinase 7 (CDK7) plays a double role as it activates several other cyclin dependent kinases and participates to the initiation of transcription. This kinase is overexpressed in various types of tumors. Relatively few selective CDK7 inhibitors have been up to now disclosed. Most of these inhibitors belong to two chemical families: pyrazolopyrimidines and pyrazolotriazines on one side and pyrimidines on another side. They also differ by their molecular mechanism of action. Some are acting as competitive inhibitors and some others are covalent inhibitors. With these tools, the understanding of the potential therapeutic interest of CDK7 inhibitors in cancer is rapidly g…

Cell SurvivalAntineoplastic Agents01 natural sciences03 medical and health sciencesDrug DevelopmentCyclin-dependent kinaseTranscription (biology)Cell Line TumorDrug DiscoverymedicineAnimalsHumansIC50Protein Kinase Inhibitors030304 developmental biologyPharmacology0303 health sciencesbiology010405 organic chemistryChemistryKinaseTriazinesOrganic ChemistryGeneral Medicinemedicine.diseaseCyclin-Dependent Kinases0104 chemical sciencesLeukemiaPyrimidinesbiology.proteinCancer researchMolecular mechanismCyclin-dependent kinase 7Cyclin-Dependent Kinase-Activating KinaseEuropean journal of medicinal chemistry
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Pyrazole[3,4-d]pyrimidine derivatives loaded into halloysite as potential CDK inhibitors

2021

Uncontrolled cell proliferation is a hallmark of cancer as a result of rapid and deregulated progression through the cell cycle. The inhibition of cyclin-dependent kinases (CDKs) activities is a promising therapeutic strategy to block cell cycle of tumor cells. In this work we reported a new example of nanocomposites based on halloysite nanotubes (HNTs)/pyrazolo[3,4-d]pyrimidine derivatives (Si306 and Si113) as anticancer agents and CDK inhibitors. HNTs/Si306 and HNTs/Si113 nanocomposites were synthesized and characterized. The release kinetics were also investigated. Antitumoral activity was evaluated on three cancer cell lines (HeLa, MDA-MB-231 and HCT116) and the effects on cell cycle ar…

Cell cycle checkpointPyrimidinePharmaceutical Science02 engineering and technologyCDK inhibitors; Halloysite; Nanocomposites; Pyrazolo[34-d]pyrimidine derivatives; Cell Cycle Checkpoints; Cell Line Tumor; Clay; Humans; Pyrazoles; PyrimidinesPyrazolo[34-d]pyrimidine derivativesPyrazole030226 pharmacology & pharmacyCell LineNanocompositesHeLa03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCyclin-dependent kinaseCell Line TumorPyrazolo[3HumansSettore BIO/06 - Anatomia Comparata E CitologiaSettore CHIM/02 - Chimica FisicaTumorbiologyChemistryKinaseCell growth4-d]pyrimidine derivativesHalloysiteSettore CHIM/06 - Chimica OrganicaCell Cycle CheckpointsCell cycle021001 nanoscience & nanotechnologybiology.organism_classificationSettore BIO/18 - GeneticaPyrimidinesSettore CHIM/03 - Chimica Generale E Inorganicabiology.proteinCancer researchClayPyrazoles0210 nano-technologyCDK inhibitors
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