Search results for "Cancer epigenetics"

showing 10 items of 11 documents

Epigenetic regulation of DNA repair genes and implications for tumor therapy

2017

DNA repair represents the first barrier against genotoxic stress causing metabolic changes, inflammation and cancer. Besides its role in preventing cancer, DNA repair needs also to be considered during cancer treatment with radiation and DNA damaging drugs as it impacts therapy outcome. The DNA repair capacity is mainly governed by the expression level of repair genes. Alterations in the expression of repair genes can occur due to mutations in their coding or promoter region, changes in the expression of transcription factors activating or repressing these genes, and/or epigenetic factors changing histone modifications and CpG promoter methylation or demethylation levels. In this review we …

0301 basic medicineGeneticsDNA RepairDNA repairHealth Toxicology and MutagenesisDNA MethylationBiologyEpigenesis Genetic03 medical and health sciences030104 developmental biology0302 clinical medicineEpigenetics of physical exerciseNeoplasms030220 oncology & carcinogenesisDNA Repair ProteinDNA methylationGeneticsCancer researchAnimalsHumansCpG IslandsDNA mismatch repairEpigeneticsCancer epigeneticsEpigenomicsMutation Research/Reviews in Mutation Research
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Resminostat plus sorafenib as second-line therapy of advanced hepatocellular carcinoma - The SHELTER study

2016

Background & Aims No established therapies for patients with hepatocellular carcinoma (HCC) and progression on first-line sorafenib treatment currently exist. This phase I/II trial investigated safety, pharmacokinetics and potential biomarkers of the histone deacetylase inhibitor resminostat and a combination therapy with resminostat and sorafenib. Methods Patients with HCC and radiologically confirmed progression on sorafenib were treated in an exploratory, multi-center, open-label, uncontrolled, non-randomized, parallel group phase I/II study. In the combination group (n=38) four dose levels ranged from daily 200 to 600mg resminostat plus 400 to 800mg sorafenib. The monotherapy group (n=1…

0301 basic medicineOncologySorafenibmedicine.medical_specialtyCombination therapymedicine.drug_classMedizinCancer epigeneticPharmacology03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCancer epigeneticsResminostatInternal medicineClinical endpointmedicineCarcinomaneoplasmsEpigenetic treatmentFirst-in-man studyHistone deacetylase inhibitorHepatologybusiness.industryHistone deacetylase inhibitormedicine.diseasedigestive system diseases030104 developmental biologyZinc finger protein 64chemistryCancer epigenetics; Drug resistance; Epigenetic treatment; Histone deacetylase inhibitor; Zinc finger protein 64030220 oncology & carcinogenesisHepatocellular carcinomaDrug resistancebusinessmedicine.drug
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Role of glutathione in the regulation of epigenetic mechanisms in disease

2017

Epigenetics is a rapidly growing field that studies gene expression modifications not involving changes in the DNA sequence. Histone H3, one of the basic proteins in the nucleosomes that make up chromatin, is S-glutathionylated in mammalian cells and tissues, making Gamma-L-glutamyl-L-cysteinylglycine, glutathione (GSH), a physiological antioxidant and second messenger in cells, a new post-translational modifier of the histone code that alters the structure of the nucleosome. However, the role of GSH in the epigenetic mechanisms likely goes beyond a mere structural function. Evidence supports the hypothesis that there is a link between GSH metabolism and the control of epigenetic mechanisms…

0301 basic medicineS-AdenosylmethionineEpigenetic regulation of neurogenesisADNBiologyBiochemistryEpigenesis GeneticHistones03 medical and health sciencesHistone H3Epigenetics of physical exerciseHistonasNeoplasmsPhysiology (medical)AnimalsHumansHistone codeEpigeneticsCancer epigeneticsEpigenomicsMetabolic SyndromeGenNeurodegenerative DiseasesDNA MethylationGlutathioneGenéticaNucleosomesMicroRNAs030104 developmental biologyBiochemistryHistone methyltransferaseProteínaEpigenéticaProtein Processing Post-TranslationalFree Radical Biology and Medicine
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Epithelial-to-mesenchymal transition in the context of epidermal growth factor receptor inhibition in non-small-cell lung cancer

2018

The identification of oncogenic driver mutations in non-small-cell lung cancer (NSCLC) has led to the development of targeted drugs. Tyrosine kinase inhibitors (TKIs) directed against the epidermal growth factor receptor (EGFR) target lung tumours bearing EGFR-activating mutations. This new therapeutic strategy has greatly improved tumour response rates. However, drug resistance invariably occurs during TKI-based treatment. Epithelial-to-mesenchymal transition (EMT) is one of the resistance mechanisms identified in EGFR-mutated NSCLC treated with TKIs. In this review we gather together the most important findings on this phenomenon in relation to cancer stem cells and cancer epigenetics. We…

0301 basic medicinebiologybusiness.industrymedicine.drug_classmedicine.disease_causemedicine.diseaseGeneral Biochemistry Genetics and Molecular BiologyTyrosine-kinase inhibitorrespiratory tract diseases03 medical and health sciences030104 developmental biology0302 clinical medicineCancer stem cell030220 oncology & carcinogenesisCancer researchmedicinebiology.proteinEpithelial–mesenchymal transitionEpidermal growth factor receptorCancer epigeneticsGeneral Agricultural and Biological SciencesCarcinogenesisbusinessLung cancerTyrosine kinaseBiological Reviews
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p53 is involved in regulation of the DNA repair gene O6-methylguanine-DNA methyltransferase (MGMT) by DNA damaging agents

1998

The DNA repair protein O6-methylguanine-DNA methyltransferase (MGMT) is inducible by genotoxic stress. MGMT induction results from transcriptional activation of the MGMT gene which is a specific response to DNA damage. A possible factor involved in triggering MGMT induction might be p53, because both p53 and MGMT are activated by DNA breaks. To study the effect of p53 on induction of the MGMT gene, we compared the presence of functional wild-type (wt) and mutant p53 with MGMT expression level in various mouse fibroblasts and rat hepatoma cell lines upon genotoxic treatment. Cells which responded to ionizing radiation (IR) by MGMT induction displayed functional p53, whereas in cells not expr…

Chloramphenicol O-AcetyltransferaseCancer ResearchMethyltransferaseDNA RepairDNA damageDNA repairRecombinant Fusion ProteinsBiologyTransfectionDNA methyltransferaseDNA AntisenseGene Expression Regulation EnzymologicMiceO(6)-Methylguanine-DNA MethyltransferaseLiver Neoplasms ExperimentalGene expressionDNA Repair ProteinTumor Cells CulturedGeneticsAnimalsCancer epigeneticsPromoter Regions GeneticneoplasmsMolecular BiologyCell NucleusMice KnockoutCell Cycle3T3 CellsTransfectionGenes p53Molecular biologydigestive system diseasesRatsCancer researchTumor Suppressor Protein p53DNA DamageOncogene
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The Histone Deacetylase Inhibitor JAHA Down-Regulates pERK and Global DNA Methylation in MDA-MB231 Breast Cancer Cells

2015

The histone deacetylase inhibitor N-1-(ferrocenyl)-N-8-hydroxyoctanediamide (JAHA) down-regulates extracellular-signal-regulated kinase (ERK) and its activated form in triple-negative MDA-MB231 breast cancer cells after 18 h and up to 30 h of treatment, and to a lesser extent AKT and phospho-AKT after 30 h and up to 48 h of treatment. Also, DNA methyltransferase 1 (DNMT1), 3b and, to a lesser extent, 3a, downstream ERK targets, were down-regulated already at 18 h with an increase up to 48 h of exposure. Methylation-sensitive restriction arbitrarily-primed (MeSAP) polymerase chain reaction (PCR) analysis confirmed the ability of JAHA to induce genome-wide DNA hypomethylation at 48 h of expos…

DNA methyltransferase (DNMT)medicine.drug_classDNA methyltransferaselcsh:TechnologymedicineGeneral Materials ScienceCancer epigeneticsSettore BIO/06 - Anatomia Comparata E Citologialcsh:Microscopyhistone deacetylase inhibitorlcsh:QC120-168.85QD0415Histone deacetylase 5lcsh:QH201-278.5extracellular-signal-regulated kinase (ERK)ChemistryHistone deacetylase 2lcsh:TCommunicationAKTHistone deacetylase inhibitorMolecular biologySettore BIO/18 - Geneticalcsh:TA1-2040DNA methylationDNMT1lcsh:Descriptive and experimental mechanicslcsh:Electrical engineering. Electronics. Nuclear engineeringlcsh:Engineering (General). Civil engineering (General)lcsh:TK1-9971DNA hypomethylationQD0241
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Methyl-CpG-binding proteins

2000

CpG methylation, the most common epigenetic modification of vertebrate genomes, is primarily associated with transcriptional repression. MeCP2, MBD1, MBD2, MBD3 and MBD4 constitute a family of vertebrate proteins that share the methyl-CpG-binding domain (MBD). The MBD, consisting of about 70 residues, possesses a unique alpha/beta-sandwich structure with characteristic loops, and is able to bind single methylated CpG pairs as a monomer. All MBDs except MBD4, an endonuclease that forms a complex with the DNA mismatch-repair protein MLH1, form complexes with histone deacetylase. It has been established that MeCP2, MBD1 and MBD2 are involved in histone deacetylase-dependent repression and it i…

GeneticsTranscription GeneticChromosomal Proteins Non-HistoneMethyl-CpG-Binding Protein 2Molecular Sequence DataDNADNA MethylationBiologyBiochemistryProtein Structure TertiaryMethyl-CpG-binding domainDNA-Binding ProteinsRepressor ProteinsEpigenetics of physical exerciseHistone methyltransferaseDNA methylationHistone methylationHistone H2AAnimalsHumansHistone codeCpG IslandsAmino Acid SequenceGene SilencingCancer epigeneticsEuropean Journal of Biochemistry
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Histone Deacetylase Inhibitors in the Treatment of Hematological Malignancies and Solid Tumors

2010

The human genome is epigenetically organized through a series of modifications to the histone proteins that interact with the DNA. In cancer, many of the proteins that regulate these modifications can be altered in both function and expression. One example of this is the family of histone deacetylases (HDACs), which as their name implies remove acetyl groups from the histone proteins, allowing for more condensed nucleosomal structure. HDACs have increased expression in cancer and are also believed to promote carcinogenesis through the acetylation and interaction with key transcriptional regulators. Given this, small molecule histone deacetylases inhibitors have been identified and developed…

Health Toxicology and Mutagenesislcsh:Biotechnologylcsh:MedicineReview ArticleNeoplasmslcsh:TP248.13-248.65GeneticsAnimalsHumansCancer epigeneticsMolecular BiologyHistone deacetylase 5biologyHDAC11Histone deacetylase 2HDAC10lcsh:RGeneral MedicineHistone Deacetylase InhibitorsHistoneBiochemistryAcetylationHematologic Neoplasmsbiology.proteinCancer researchMolecular MedicineHistone deacetylaseBiotechnologyJournal of Biomedicine and Biotechnology
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Induced Pluripotent Mesenchymal Stromal Cell Clones Retain Donor-derived Differences in DNA Methylation Profiles

2012

Reprogramming of somatic cells into induced pluripotent stem cells (iPSCs) is an epigenetic phenomenon. It has been suggested that iPSC retain some tissue-specific memory whereas little is known about interindividual epigenetic variation. We have reprogrammed mesenchymal stromal cells from human bone marrow (iP-MSC) and compared their DNA methylation profiles with initial MSC and embryonic stem cells (ESCs) using high-density DNA methylation arrays covering more than 450,000 CpG sites. Overall, DNA methylation patterns of iP-MSC and ESC were similar whereas some CpG sites revealed highly significant differences, which were not related to parental MSC. Furthermore, hypermethylation in iP-MSC…

Induced Pluripotent Stem CellsBiologyDrug DiscoveryGeneticsHumansEpigeneticsCancer epigeneticsInduced pluripotent stem cellMolecular BiologyPharmacologyMesenchymal Stromal CellsReverse Transcriptase Polymerase Chain ReactionMesenchymal Stem CellsMethylationDNA MethylationFlow CytometryMolecular biologyEmbryonic stem cellImmunohistochemistryClone CellsCpG siteDNA methylationMolecular MedicineOriginal ArticleCpG IslandsReprogrammingMolecular Therapy
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Release of Hypoacetylated and Trimethylated Histone H4 Is an Epigenetic Marker of Early Apoptosis

2006

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PhysiologyFisiologiaHL-60 CellsApoptosisDNA FragmentationBiologyBiochemistryHistonesHistone H4Jurkat CellsHistone H1HeterochromatinHistone methylationHistone H2AHumansHistone codeCancer epigeneticsMolecular BiologyEpigenomicsApoptosiDNACell BiologyMetabolismeMetabolismHistone methyltransferaseCancer researchBiomarkersJournal of Biological Chemistry
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