Search results for "DNA Modification Methylases"

showing 10 items of 20 documents

Methylation of cytokines gene promoters in IL-1β-treated human intestinal epithelial cells

2017

Objective and design: Epigenetic regulation is important in the activation of inflammatory cells. In the present study, we evaluated if DNA-methylation variations are involved in Interleukin-1β (IL-1β)-induced intestinal epithelial cells activation. Materials and methods: Differentiated Caco-2 cells were exposed to IL-1β or to 5-azadeoxycytidine (5-azadC) for 24 or 48 h. Genome-wide methylation status was evaluated, while DNA methylation status at the promoter region of the gene encoding interleukin-6, 8 and 10 (IL-6, 8 and 10) was estimated. The levels of the corresponding gene products as well as DNA methyltransferases (DNMTs) quantity were assessed. Results: IL-1β decreased genomic m…

0301 basic medicineMethyltransferaseInterleukin-1betaImmunologyEpigenesis GeneticCaco-2 cell03 medical and health sciences0302 clinical medicineSettore BIO/13 - Biologia ApplicataSettore BIO/10 - BiochimicaHumansIL-1βEpigeneticsInterleukin 8Intestinal MucosaPromoter Regions GeneticDNA Modification MethylasesGeneInflammationPharmacologyDNA methylationChemistryInterleukinsPromoterMethylationMolecular biologySettore BIO/18 - Genetica030104 developmental biology030220 oncology & carcinogenesisDNA methylationDNMT1Caco-2 CellsInflammation MediatorsInflammation Research
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Schlafen-11 (SLFN11): a step forward towards personalized medicine in small-cell lung cancer?

2018

Purpose Both temozolomide (TMZ) and poly (ADP-ribose) polymerase (PARP) inhibitors are active in small-cell lung cancer (SCLC). This phase II, randomized, double-blind study evaluated whether addition of the PARP inhibitor veliparib to TMZ improves 4-month progression-free survival (PFS). Patients and Methods A total of 104 patients with recurrent SCLC were randomly assigned 1:1 to oral veliparib or placebo 40 mg twice daily, days 1 to 7, and oral TMZ 150 to 200 mg/m

0301 basic medicineOncologyMaleLung NeoplasmsDNA Mutational AnalysisPoly (ADP-Ribose) Polymerase-1Placebos0302 clinical medicineAntineoplastic Combined Chemotherapy ProtocolsPromoter Regions GeneticDNA Modification MethylasesAged 80 and overStandard treatmentNuclear ProteinsMiddle AgedNeoplastic Cells CirculatingImmunohistochemistryhumanitiesEditorialOncology030220 oncology & carcinogenesisFemaleNon small cellAdultmedicine.medical_specialtyMEDLINEAggressive disease03 medical and health sciencesText miningDouble-Blind MethodInternal medicinemedicineBiomarkers TumorTemozolomideHumansLung cancerneoplasmsAntineoplastic Agents AlkylatingAgedbusiness.industryTumor Suppressor ProteinsDNA Methylationmedicine.diseaseSmall Cell Lung Carcinomarespiratory tract diseases030104 developmental biologyDNA Repair EnzymesBenzimidazolesPersonalized medicinebusiness
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Chemoradiotherapy of Newly Diagnosed Glioblastoma With Intensified Temozolomide

2009

Purpose To evaluate the toxicity and efficacy of chemoradiotherapy with temozolomide (TMZ) administered in an intensified 1-week on/1-week off schedule plus indomethacin in patients with newly diagnosed glioblastoma. Patients and Methods A total of 41 adult patients (median Karnofsky performance status, 90%; median age, 56 years) were treated with preirradiation TMZ at 150 mg/m 2 (1 week on/1 week off), involved-field radiotherapy combined with concomitant low-dose TMZ (50 mg/m 2 ), maintenance TMZ starting at 150 mg/m 2 using a 1-week on/1-week off schedule, plus maintenance indomethacin (25 mg twice daily). Results The median follow-up interval was 21.7 months. Grade 4 hematologic toxicit…

AdultMaleOncologyCancer Researchmedicine.medical_specialtymedicine.medical_treatmentIndomethacinDisease-Free SurvivalDrug Administration ScheduleGermanyInternal medicineConfidence IntervalsTemozolomidemedicineHumansRadiology Nuclear Medicine and imagingProspective StudiesKarnofsky Performance StatusAntineoplastic Agents AlkylatingDNA Modification MethylasesSurvival rateAgedChemotherapyRadiationTemozolomideBrain Neoplasmsbusiness.industryTumor Suppressor ProteinsAnti-Inflammatory Agents Non-SteroidalDNA MethylationMiddle AgedCombined Modality TherapyConfidence intervalSurgeryDacarbazineSurvival RateRegimenDNA Repair EnzymesOncologyConcomitantToxicityFemaleGlioblastomabusinessChemoradiotherapyFollow-Up Studiesmedicine.drugInternational Journal of Radiation Oncology*Biology*Physics
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NOA-05 phase 2 trial of procarbazine and lomustine therapy in gliomatosis cerebri.

2011

The NOA-05 multicenter trial was performed to analyze the efficacy of primary chemotherapy with procarbazine and lomustine (PC) in patients with gliomatosis cerebri (GC) and to define clinical, imaging, and molecular factors influencing outcome.Thirty-five patients with previously untreated GC were treated with up to six 56-day courses of 110mg/m(2) lomustine on day 1 and 60mg/m(2) procarbazine on days 8 to 21. The primary endpoint was the rate of patients without therapy failure (defined as progressive disease, death from any cause, or termination of PC therapy before the end of course 4) at 8 months after the beginning of PC chemotherapy.The failure-free survival rate at 8 months was 50.3…

AdultMalemedicine.medical_specialtyEndpoint DeterminationGliomatosis cerebriAntineoplastic AgentsGene mutationProcarbazineGastroenterologyDisease-Free SurvivalLomustineInternal medicineMulticenter trialAntineoplastic Combined Chemotherapy ProtocolsBiomarkers TumorMedicineHumansProspective StudiesKarnofsky Performance StatusSurvival rateDNA Modification MethylasesAgedbusiness.industryTumor Suppressor ProteinsHazard ratioBrainLomustineMiddle Agedmedicine.diseasePrognosisCombined Modality TherapyMagnetic Resonance ImagingNeoplasms NeuroepithelialSurvival AnalysisSurgeryDNA Repair EnzymesTreatment OutcomeNeurologyProcarbazineSample SizeDisease ProgressionFemaleNeurology (clinical)businessProgressive diseasemedicine.drugAnnals of neurology
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Activity and safety of temozolomide in advanced adrenocortical carcinoma patients

2019

Objective Temozolomide has shown a significant anti-proliferative activity on adrenocortical cancer (ACC) cells in vitro. Design On the basis of these results the drug was prescribed as second/third line in advanced metastatic ACC patients in four referral centers in Italy. Methods We retrospectively collected anagraphic, clinical and pathological data of patients with advanced ACC with disease progression to standard chemotherapy plus mitotane who were treated with temozolomide at the dose of 200 mg/m2/die given for 5 consecutive days every 28 days. The primary endpoint was the disease control rate, defined as objective response or disease stabilization after 3 months. Secondary endpoints…

AdultOncologymedicine.medical_specialtytemozolomide adrenocortical carcinomaDisease ResponseSettore MED/06 - Oncologia MedicaEndocrinology Diabetes and Metabolismmedicine.medical_treatment030209 endocrinology & metabolism03 medical and health sciences0302 clinical medicineEndocrinologyStable DiseaseInternal medicineAdrenocortical CarcinomaTemozolomideClinical endpointHumansMedicineAdrenocortical carcinomaMitotaneDNA Modification MethylasesAgedRetrospective StudiesChemotherapyTemozolomidebusiness.industryTumor Suppressor ProteinsRetrospective cohort studyGeneral MedicineMiddle Agedmedicine.diseaseDNA Repair EnzymesEndocrinology030220 oncology & carcinogenesisbusinessmedicine.drug
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MGMT: Key node in the battle against genotoxicity, carcinogenicity and apoptosis induced by alkylating agents

2007

O(6)-methylguanine-DNA methyltransferase (MGMT) plays a crucial role in the defense against alkylating agents that generate, among other lesions, O(6)-alkylguanine in DNA (collectively termed O(6)-alkylating agents [O(6)AA]). The defense is highly important, since O(6)AA are common environmental carcinogens, are formed endogenously during normal cellular metabolism and possibly inflammation, and are being used in cancer therapy. O(6)AA induced DNA damage is subject to repair, which is executed by MGMT, AlkB homologous proteins (ABH) and base excision repair (BER). Although this review focuses on MGMT, the mechanism of repair by ABH and BER will also be discussed. Experimental systems, in wh…

Alkylating AgentsMethyltransferaseAlkylationDNA RepairDNA repairDNA damageGene ExpressionApoptosisIn Vitro TechniquesBiologyDNA Mismatch RepairModels BiologicalBiochemistryNecrosisO(6)-Methylguanine-DNA MethyltransferaseNeoplasmsAnimalsHumansDNA Modification MethylasesneoplasmsMolecular BiologyCarcinogenChromosome AberrationsGeneticsTumor Suppressor ProteinsO-6-methylguanine-DNA methyltransferaseDNACell BiologyBase excision repairdigestive system diseasesDNA Repair EnzymesMutationCancer researchDNA mismatch repairSister Chromatid ExchangeDNA DamageAlkyltransferaseDNA Repair
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Why do results conflict regarding the prognostic value of the methylation status in colon cancers? The role of the preservation method.

2012

Abstract Background In colorectal carcinoma, extensive gene promoter hypermethylation is called the CpG island methylator phenotype (CIMP). Explaining why studies on CIMP and survival yield conflicting results is essential. Most experiments to measure DNA methylation rely on the sodium bisulfite conversion of unmethylated cytosines into uracils. No study has evaluated the performance of bisulfite conversion and methylation levels from matched cryo-preserved and Formalin-Fixed Paraffin Embedded (FFPE) samples using pyrosequencing. Methods Couples of matched cryo-preserved and FFPE samples from 40 colon adenocarcinomas were analyzed. Rates of bisulfite conversion and levels of methylation of …

Cancer ResearchBisulfite sequencing[SDV.CAN]Life Sciences [q-bio]/CancerAdenocarcinomaBiologyMLH1lcsh:RC254-282[ SDV.CAN ] Life Sciences [q-bio]/Cancerchemistry.chemical_compound[SDV.CAN] Life Sciences [q-bio]/CancerPredictive Value of TestsBiomarkers TumorGeneticsHumansSulfitesDNA Modification MethylasesAdaptor Proteins Signal TransducingCryopreservationParaffin EmbeddingTumor Suppressor ProteinsNuclear ProteinsReproducibility of ResultsDNA NeoplasmMethylationDNA MethylationPrognosislcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensMolecular biologydigestive system diseasesNeoplasm ProteinsBisulfiteDNA Repair EnzymesLong Interspersed Nucleotide ElementsPhenotypeOncologyCpG sitechemistrySodium bisulfiteColonic NeoplasmsDNA methylationFeasibility StudiesPyrosequencingCpG IslandsMutL Protein Homolog 1Research Article
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Temozolomide- and fotemustine-induced apoptosis in human malignant melanoma cells: response related to MGMT, MMR, DSBs, and p53

2009

Malignant melanomas are highly resistant to chemotherapy. First-line chemotherapeutics used in melanoma therapy are the methylating agents dacarbazine (DTIC) and temozolomide (TMZ) and the chloroethylating agents BCNU and fotemustine. Here, we determined the mode of cell death in 11 melanoma cell lines upon exposure to TMZ and fotemustine. We show for the first time that TMZ induces apoptosis in melanoma cells, using therapeutic doses. For both TMZ and fotemustine apoptosis is the dominant mode of cell death. The contribution of necrosis to total cell death varied between 10 and 40%. The O(6)-methylguanine-DNA methyltransferase (MGMT) activity in the cell lines was between 0 and 1100 fmol m…

Cancer ResearchProgrammed cell deathDNA repairDacarbazineBlotting WesternApoptosistemozolomideBiologyCollagen Type XIDNA Mismatch RepairNecrosisGliomaAntineoplastic Combined Chemotherapy ProtocolsTumor Cells CulturedmedicineHumansDNA Breaks Double-StrandedEverolimusPhosphorylationDNA Modification MethylasesMelanomaneoplasmsSirolimusTemozolomideTumor Suppressor ProteinsMelanomafotemustinemelanoma therapymedicine.diseaseDacarbazineEnzyme Activationmismatch repairDNA Repair EnzymesOncologyApoptosisCaspasesCancer researchFotemustineTumor Suppressor Protein p53Translational TherapeuticsMGMTmedicine.drugBritish Journal of Cancer
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MGMT activity, promoter methylation and immunohistochemistry of pretreatment and recurrent malignant gliomas: a comparative study on astrocytoma and …

2010

The DNA repair protein O(6)-methylguanine-DNA methyltransferase (MGMT) is a key player in tumor cell resistance. Promoter methylation, MGMT activity and immunohistochemistry are used for determining the MGMT status. However, it is unclear whether MGMT promoter methylation correlates with MGMT activity and whether MGMT promoter methylation of the pretreatment tumor predicts the MGMT status of recurrences. To address these questions, we determined MGMT activity promoter methylation and immunoreactivity in pretreatment and recurrent glioblastomas (GB, WHO Grade IV), and in astrocytomas (WHO Grade III). We show that GB that were promoter methylated display a range of 0-62 fmol/mg MGMT and tumor…

Cancer Researchmedicine.medical_specialtyPathologyMethyltransferaseDNA repairAstrocytomaBiologyRecurrenceCell Line TumormedicineHumansPromoter Regions GeneticDNA Modification MethylasesneoplasmsBrain NeoplasmsTumor Suppressor ProteinsAstrocytomaCancerAnatomical pathologyBiological activityMethylationDNA Methylationmedicine.diseaseImmunohistochemistrydigestive system diseasesDNA Repair EnzymesOncologyCancer researchImmunohistochemistryGlioblastomaInternational Journal of Cancer
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Novel Approaches for Glioblastoma Treatment: Focus on Tumor Heterogeneity, Treatment Resistance, and Computational Tools

2019

BACKGROUND: Glioblastoma (GBM) is a highly aggressive primary brain tumor. Currently, the suggested line of action is the surgical resection followed by radiotherapy and treatment with the adjuvant temozolomide (TMZ), a DNA alkylating agent. However, the ability of tumor cells to deeply infiltrate the surrounding tissue makes complete resection quite impossible, and in consequence, the probability of tumor recurrence is high, and the prognosis is not positive. GBM is highly heterogeneous and adapts to treatment in most individuals. Nevertheless, these mechanisms of adaption are unknown. RECENT FINDINGS: In this review, we will discuss the recent discoveries in molecular and cellular heterog…

Cancer Researchmedicine.medical_treatmentDNA Mutational AnalysisBrain tumorBioinformaticsComplete resectionTumor heterogeneityCancer VaccinesMicrotubulesArticleClonal EvolutionMachine LearningGenetic HeterogeneityCancer stem cellAntineoplastic Combined Chemotherapy ProtocolsTumor MicroenvironmentMedicineHumansTreatment resistancePrecision MedicineDNA Modification MethylasesImmune Checkpoint InhibitorsTemozolomideModels Geneticbusiness.industryBrain NeoplasmsTumor Suppressor ProteinsBrainComputational BiologyChemoradiotherapy Adjuvantmedicine.diseasePrognosisRadiation therapyDNA Repair EnzymesOncologyDrug Resistance NeoplasmMutationTumor Suppressor Protein p53businessGlioblastomaGlioblastomamedicine.drug
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