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  • GENE  (35)
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  • 1
    Keywords: EXPRESSION ; SURVIVAL ; NETWORK ; NETWORKS ; GENE ; LINKAGE ; SUSCEPTIBILITY ; LYMPHOMA ; MALIGNANCIES ; genetics ; molecular ; FEATURES ; MALIGNANCY ; REGRESSION ; review ; FAMILIES ; CANDIDATE GENES ; CLL ; PREDISPOSITION ; leukaemia ; USA ; ENGLAND ; EXPANSION ; chronic lymphocytic leukaemia ; B-CELL LYMPHOCYTOSIS ; CHALLENGES ; family studies ; genetic association
    Abstract: Although the familial aspect of chronic lymphocytic leukaemia (CLL) has been appreciated for decades, it is only with the recent confluence of improved molecular and gene technologies and world-wide collaborative networks that accelerated progress has become apparent. In this summary we highlight selected themes in the genetics of CLL emphasizing the opportunities and challenges of this malignancy
    Type of Publication: Journal article published
    PubMed ID: 18021078
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  • 2
    Keywords: APOPTOSIS ; CANCER ; EXPRESSION ; GROWTH ; GROWTH-FACTOR ; SURVIVAL ; tumor ; carcinoma ; CELL ; Germany ; PATHWAY ; DIAGNOSIS ; RISK ; GENE ; GENES ; SAMPLE ; SAMPLES ; PATIENT ; DNA ; MARKER ; RISK-FACTORS ; CELL-LINES ; DOWN-REGULATION ; EXPRESSION ANALYSIS ; ASSAY ; risk factors ; RATES ; CELL-LINE ; DNA methylation ; MARKERS ; SIGNALING PATHWAY ; HOMOLOG ; BETA ; HEAD ; squamous cell carcinoma ; GROWTH-FACTOR-BETA ; OVEREXPRESSION ; HYPOXIA ; NECK-CANCER ; signaling ; CELL CARCINOMA ; ONCOLOGY ; RE ; TUMOR-SUPPRESSOR ; TUMORIGENESIS ; CANDIDATE GENES ; TRANSPORTER ; analysis ; SUPPRESSOR ; USA ; CANDIDATE ; cancer research ; RISK-FACTOR ; CANCERS ; B-CELL ; DNA-METHYLATION ; modification ; tumor suppressor ; epigenetic
    Abstract: Head and neck squamous cell carcinoma (HNSCC) is a very aggressive cancer. In advanced stages, the patient has poor chances of receiving effective treatment, and survival rates are low. To facilitate timely diagnosis and improve treatment, elucidation of early detection markers is crucial. DNA methylation markers are particularly advantageous because DNA methylation is an early event in tumorigenesis, and the epigenetic modification, 5-methylcytosine, is a stable mark. A genome-wide screen using Restriction Landmark Genomic Scanning found a set of genes that are most commonly methylated in head and neck cancers. Five candidate genes: septin 9 (SEPT9), sodium-coupled monocarboxylate transporter 1 (SLM8), functional smad-suppressing element on chromosome 18 (FUSSEL18), early B-cell factor 3 (EBF3), and iroquois homeobox 1 (IRX1) were methylated in 27% to 67% of the HNSCC patient samples tested. Furthermore, similar to 50% of the methylated tumor samples shared methylation between two of the five genes (most commonly between EBF3 and IRX-1), and 15% shared methylation between three of the five genes. Expression analysis revealed candidate gene down-regulation in 25% to 93% of the HNSCC samples, and 5-aza-2'-deoxycytidine treatment was able to restore expression in at least 2 of 5 HNSCC cell lines for all of the genes tested. Overexpression of the three most frequently down-regulated candidates, SLC5A8, IRX1, and EBF3, validated their tumor suppressor potential by growth curve analysis and colony formation assay. Interestingly, all of the candidates identified may be involved in the transforming growth factor beta signaling pathway, which is often disrupted in HNSCC
    Type of Publication: Journal article published
    PubMed ID: 18559491
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  • 3
    Keywords: CANCER ; CELLS ; EXPRESSION ; INHIBITOR ; tumor ; BLOOD ; CELL ; DEATH ; GENE ; GENE-EXPRESSION ; GENES ; LINES ; DNA ; MECHANISM ; CELL-LINES ; ACID ; TRANSPORT ; CHROMATIN ; chromatin remodeling ; gene expression ; CELL-DEATH ; PROMOTER ; CELL-LINE ; leukemia ; LINE ; DNA methylation ; acetylation ; HISTONE DEACETYLASE ; histone deacetylase inhibitor ; METHYLATION ; HYPERMETHYLATION ; NORMAL CYTOGENETICS ; TUMOR-SUPPRESSOR ; METHYLTRANSFERASE ; REARRANGEMENT ; TRANSPORTER ; ADULT PATIENTS ; cell death ; SUPPRESSOR ; PROMOTER HYPERMETHYLATION ; USA ; DECITABINE ; H4 ; GROUP-B ; DNA-METHYLATION ; response ; tumor suppressor ; epigenetic ; ABERRANT METHYLATION ; PARTIAL TANDEM DUPLICATION ; ALL-1
    Abstract: Posttranslationally modified histones and DNA hypermethylation frequently interplay to deregulate gene expression in cancer. We report that acute myeloid leukemia (AML) with an aberrant histone methyltransferase, the mixed lineage leukemia partial tandem duplication (MLL-PTD), exhibits increased global DNA methylation versus AML with MLL-wildtype (MLL-WT-, P =.02). Among the differentially methylated genes, the SLC5A8 tumor suppressor gene (TSG) was more frequently hypermethylated (P =.003). In MLL-PTD+ cell lines having SLC5A8 promoter hypermethylation, incubation with decitabine activated SLC5A8 expression. Ectopic SLC5A8 expression enhanced histones H3 and H4 acetylation in response to the histone deacetylase inhibitor, valproate, consistent with the encoded protein-SMCT1-short-chain fatty acid transport function. In addition, enhanced cell death was observed in SMCT1-expressing MLL-PTD+ AML cells treated with valproate. Within the majority of MLL-PTD AML is a mechanism in which DNA hypermethylation silences a TSG that, together with MLL-PTD, can contribute further to aberrant chromatin remodeling and altered gene expression
    Type of Publication: Journal article published
    PubMed ID: 18566324
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  • 4
    Keywords: CANCER ; EXPRESSION ; INHIBITOR ; proliferation ; CELL ; CELL-PROLIFERATION ; human ; QUANTIFICATION ; SYSTEM ; SYSTEMS ; TOOL ; DISEASE ; DISEASES ; GENE ; GENE-EXPRESSION ; SAMPLE ; SAMPLES ; TISSUE ; DNA ; MECHANISM ; TISSUES ; mechanisms ; BIOLOGY ; SEQUENCE ; SEQUENCES ; DISORDER ; SCHIZOPHRENIA ; NEOPLASIA ; PATTERNS ; gene expression ; DISRUPTION ; genetics ; REPRODUCIBILITY ; EFFICACY ; DNA methylation ; INSTABILITY ; UNITED-STATES ; ELECTROPHORESIS ; sensitivity ; METHYLATION ; GENOMIC INSTABILITY ; HYPERMETHYLATION ; INHIBITORS ; molecular biology ; HUMAN CANCER ; 5-methylcytosine ; cell proliferation ; CPG ISLANDS ; TECHNOLOGY ; microfluidics ; USA ; ACCURATE ; CANCER GENETICS ; epigenetic ; STATE ; Genetic ; ISLANDS ; RESTRICTION ; DNA/analysis/chemistry/genetics *DNA Methylation DNA Restriction Enzymes Electrophoresis,Polyacrylam ; METHYLATION INHIBITOR
    Abstract: DNA methylation is the best-studied epigenetic modification, and in mammals it describes the conversion of cytosine to 5-methylcytosine in the context of CpG dinucleotides. In recent years, it has become evident that epigenetic mechanisms are severely disrupted in human neoplasia, and evidence suggests that alterations of DNA methylation patterns may be an integral mechanism in the etiology of other diseases such as bipolar disorder and schizophrenia. The main effect of altered DNA methylation is the disruption of normal patterns of gene expression through genomic instability and hypermethylation of CpG islands, which together could lead to uncontrolled cell proliferation. DNA methylation can be reversed through pharmacological intervention via the systemic administration of DNA methylation inhibitors. Thus, the ability to accurately quantify DNA methylation levels in genomic sequences is a prerequisite to assess not only treatment efficacy, but also the effect of the DNA methylation inhibitors on bystander tissues. Several methods are currently available for the analysis of DNA methylation. Nonetheless, accurate and reproducible quantification of DNA methylation remains challenging. Here, we describe Bio-COBRA, a modified protocol for combined bisulfite restriction analysis (COBRA) that incorporates an electrophoresis step in microfluidics chips. Microfluidics technology involves the handling of small amounts of liquid in miniaturized systems. Bio-COBRA provides a platform for the rapid and quantitative assessment of DNA methylation patterns in large sample sets. Its sensitivity and reproducibility also make it an excellent tool for the analysis of DNA methylation in clinical samples
    Type of Publication: Journal article published
    PubMed ID: 18987820
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  • 5
    Keywords: CANCER ; CELLS ; CELL ; SUPPORT ; SITES ; GENE ; GENOME ; SAMPLE ; SURGERY ; DNA ; BIOLOGY ; MOLECULAR-BIOLOGY ; SEQUENCE ; SEQUENCES ; RECOGNITION ; COPY NUMBER ; DNA methylation ; DISPLAY ; UNITED-STATES ; ELECTROPHORESIS ; METHYLATION ; SINGLE ; molecular biology ; CPG ISLANDS ; PROFILES ; TECHNOLOGY ; SEPARATION ; USA ; GENOMES ; CALIFORNIA ; epigenetic ; STATE ; Genetic ; ISLANDS ; RESTRICTION ; Animals Brain Neoplasms/chemistry/genetics *CpG Islands DNA/analysis/chemistry/genetics DNA Fingerpr ; GENE COPY NUMBER
    Abstract: Restriction landmark genomic scanning (RLGS) is a method that provides a quantitative genetic and epigenetic (cytosine methylation) assessment of thousands of CpG islands in a single gel without prior knowledge of gene sequence. The method is based on two-dimensional separation of radiolabeled genomic DNA into nearly 2,000 discrete fragments that have a high probability of containing gene sequences. Genomic DNA is digested with an infrequently cutting restriction enzyme, such as NotI or AscI, radiolabeled at the cleaved ends, digested with a second restriction enzyme, and then electrophoresed through a narrow, 60-cm-long agarose tube-shaped gel. The DNA in the tube gel is then digested by a third, more frequently cutting restriction enzyme and electrophoresed, in a direction perpendicular to the first separation, through a 5% nondenaturing polyacrylamide gel, and the gel is autoradiographed. Radiolabeled NotI or AscI sites are frequently used as "landmarks" because NotI or AscI cannot cleave methylated sites and since an estimated 89% and 83% of the recognition sites, respectively, are found within CpG islands. Using a methylation-sensitive enzyme, the technique has been termed RLGS-M. The resulting RLGS profile displays both the copy number and methylation status of the CpG islands. Integrated with high-resolution gene copy-number analyses, RLGS enables one to define genetic or epigenetic alteration in cells. These profiles are highly reproducible and are therefore amenable to inter- and intraindividual DNA sample comparisons. RLGS was the first of many technologies to allow large-scale DNA methylation analysis of CpG islands
    Type of Publication: Journal article published
    PubMed ID: 18987812
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  • 6
    Keywords: APOPTOSIS ; CANCER ; CELLS ; EXPRESSION ; tumor ; CELL ; human ; MODEL ; DISEASE ; SITES ; GENE ; GENES ; transcription ; MICE ; NF-KAPPA-B ; COMPLEX ; COMPLEXES ; DNA ; MECHANISM ; murine ; TRANSCRIPTION FACTOR ; IMPACT ; animals ; mechanisms ; BINDING ; SEQUENCE ; SEQUENCES ; TARGET ; MOUSE ; STAGE ; TRANSCRIPTION FACTORS ; PROGRESSION ; MALIGNANCIES ; PATTERNS ; PROMOTER ; AGE ; transgenic ; leukemia ; DNA methylation ; TUMOR-SUPPRESSOR GENE ; REGION ; B-CELLS ; RECRUITMENT ; STRATEGIES ; MOUSE MODEL ; TARGETS ; REPRESSION ; METHYLATION ; TRANSCRIPTIONAL REPRESSION ; REGULATOR ; MALIGNANCY ; PROGRAM ; TUMOR-SUPPRESSOR ; CLL ; MURINE MODEL ; development ; BINDING-SITE ; USA ; EPIGENETICS ; ONSET ; CPG-ISLAND METHYLATION ; BINDING-SITES ; OCCURS ; tumor suppressor ; epigenetic ; STATE ; BINDING SITE ; histone modifications ; ABERRANT METHYLATION ; 3 ; therapeutic ; THERAPEUTIC TARGET ; WELL ; STRATEGY ; INVESTIGATE ; RATIONALE ; TRANSCRIPTION-FACTOR ; FOXD3
    Abstract: Epigenetic alterations, including gain or loss of DNA methylation, are a hallmark of nearly every malignancy. Changes in DNA methylation can impact expression of cancer-related genes including apoptosis regulators and tumor suppressors. Because such epigenetic changes are reversible, they are being aggressively investigated as potential therapeutic targets. Here we use the E mu-TCL1 transgenic mouse model of chronic lymphocytic leukemia (CLL) to determine the timing and patterns of aberrant DNA methylation, and to investigate the mechanisms that lead to aberrant DNA methylation. We show that CLL cells from E mu-TCL1 mice at various stages recapitulate epigenetic alterations seen in human CLL. Aberrant methylation of promoter sequences is observed as early as 3 months of age in these animals, well before disease onset. Abnormally methylated promoter regions include binding sites for the transcription factor FOXD3. We show that loss of Foxd3 expression due to an NF-kappa B p50/p50:HDAC1 repressor complex occurs in TCL1-positive B cells before methylation. Therefore, specific transcriptional repression is an early event leading to epigenetic silencing of target genes in murine and human CLL. These results provide strong rationale for the development of strategies to target NF-kappa B components in CLL and potentially other B-cell malignancies
    Type of Publication: Journal article published
    PubMed ID: 19666576
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  • 7
    Keywords: EXPRESSION ; TOXICITY ; VITRO ; DISEASE ; GENE ; GENES ; PATIENT ; DNA ; CYCLE ; TARGET ; TRIAL ; LYMPHOMA ; MALIGNANCIES ; DNA methylation ; ESCALATION ; METHYLATION ; HYPERMETHYLATION ; ACUTE MYELOID-LEUKEMIA ; non-Hodgkin lymphoma ; PHASE ; DECITABINE ; B-CELL ; chronic lymphocytic leukaemia ; hematopoietic malignancies ; 5-AZA-2'-DEOXYCYTIDINE ; non-Hodgkin ; epigenetic silencing ; HENT1 ; KINASE CPG ISLAND
    Abstract: P〉Targeting aberrant DNA hypermethylation in chronic lymphocytic leukaemia (CLL) and non-Hodgkin lymphoma (NHL) with decitabine may reverse epigenetic silencing in B-cell malignancies. Twenty patients were enrolled in two phase I trials to determine the minimum effective pharmacological dose of decitabine in patients with relapsed/refractory CLL (n = 16) and NHL (n = 4). Patients received 1-3 cycles of decitabine. Dose-limiting toxicity (DLT) was observed in 2 of 4 CLL and 2 of 2 NHL patients receiving decitabine at 15 mg/m2 per d days 1-10, consisting of grade 3-4 thrombocytopenia and hyperbilirubinaemia. Six patients with CLL received decitabine at 10 mg/m2 per d days 1-10 without DLT; however, re-expression of methylated genes or changes in global DNA methylation were not observed. Therefore, a 5-day decitabine schedule was examined. With 15 mg/m2 per d decitabine days 1-5, DLT occurred in 2 of 6 CLL and 2 of 2 NHL patients, consisting of grade 3-4 neutropenia, thrombocytopenia, and febrile neutropenia. Eight patients had stable disease. In 17 patients, there were no significant changes in genome-wide methylation or in target gene re-expression. In conclusion, dose-limiting myelosuppression and infectious complications prevented dose escalation of decitabine to levels associated with changes in global methylation or gene re-expression in CLL and NHL
    Type of Publication: Journal article published
    PubMed ID: 20456354
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  • 8
    Keywords: CANCER ; CELLS ; EXPRESSION ; IN-VITRO ; INHIBITOR ; tumor ; TUMOR-CELLS ; carcinoma ; CELL ; COMBINATION ; MODEL ; VITRO ; SITE ; SITES ; GENE ; GENE-EXPRESSION ; GENES ; PROTEIN ; TISSUE ; LINES ; DNA ; CARCINOGENESIS ; BREAST ; breast cancer ; BREAST-CANCER ; PROGRESSION ; genetics ; DNA methylation ; inactivation ; PCR ; REGION ; TRANSFORMATION ; EPITHELIAL-CELLS ; CARCINOMAS ; NETHERLANDS ; histone deacetylase inhibitor ; METHYLATION ; HYPERMETHYLATION ; ESTRADIOL ; PATTERN ; SCIENCE ; CPG ISLANDS ; ESTROGEN ; 17-BETA-ESTRADIOL ; EPIGENETIC CHANGES ; MESENCHYMAL TRANSITION ; Genetic ; heregulin ; Cell transformation ; ERBB RECEPTOR FAMILY ; HISTONE-DEACETYLASE INHIBITORS ; Neuregulin
    Abstract: Epigenetic inactivation of genes by DNA hypermethylation plays an important role in carcinogenesis An in vitro model of human breast epithelial cell transformation was used to study epigenetic changes induced by estradiol during the neoplastic process Different stages of tumor initiation and progression are represented in this model being MCF-10F the normal stage; trMCF cells, the transformed stage, bsMCF cells, the invasive stage and, caMCF cells, the tumor stage Global methylation studies by restriction landmark genomic scanning (RLGS) showed an increased DNA methylation during the in the invasive and tumor stages Expression studies showed that NRG1 (neuregulin 1), CSS3 (chondroitin sulfate synthase 3) and SNIP (SNAP-25-interacting protein) were downregulated in the invasive and tumor cells. The transformed cells showed low expression of STXBP6(amysin)compared to the parental cells MCF-10F The treatment of these cells with the demethylating agent 5-aza-dC alone or in combination with the histone deacetylase inhibitor trichostatin increased the expression of NRG1, STXBP6, CSS3 and SNIP confirming that DNA methylation plays an Important role in the regulation of the expression of these genes The NRG1 exon 1 has a region located between -136 and +79 (considering +1, the translational initiation site) rich in CpG sites that was analyzed by methylation specific PCR (MSP) NRG1 exon 1 showed progressive changes in the methylation pattern associated with the progression of the neoplastic process in this model; NRG1 exon 1 was unmethylated in MCF-10F and trMCF cells, becoming hypermethylated in the invasive (bsMCF) and tumor (caMCF) stages Studies of human breast tissue samples showed that NRG1 exon 1 was partially methylated in 14 out of 17 (82.4%) invasive carcinomas although it was unmethylated in normal tissues (8 out of 10 normal breast tissue samples) Furthermore, NRG1 exon 1 was partially methylated in 9 out of 14(64.3%) morphologically normal tissue samples adjacent to invasive carcinomas. (C) 2010 Elsevier B V. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 20193695
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  • 9
    Keywords: APOPTOSIS ; CANCER ; EXPRESSION ; proliferation ; SURVIVAL ; DISEASE ; GENE ; DIFFERENTIATION ; PATHOGENESIS ; B-CELLS ; CHRONIC LYMPHOCYTIC-LEUKEMIA ; ANIMAL-MODELS ; TUMOR-SUPPRESSOR ; fludarabine ; MURINE MODEL ; B-CELL LYMPHOCYTOSIS ; LIPOPROTEIN-LIPASE
    Abstract: Inhibitor of DNA binding protein 4 (ID4) is a member of the dominant-negative basic helix-loop-helix transcription factor family that lacks DNA binding activity and has tumor suppressor function. ID4 promoter methylation has been reported in acute myeloid leukemia and chronic lymphocytic leukemia (CLL), although the expression, function, and clinical relevance of this gene have not been characterized in either disease. We demonstrate that the promoter of ID4 is consistently methylated to various degrees in CLL cells, and increased promoter methylation in a univariable analysis correlates with shortened patient survival. However, ID4 mRNA and protein expression is uniformly silenced in CLL cells irrespective of the degree of promoter methylation. The crossing of ID4(+/-) mice with E mu-TCL1 mice triggers a more aggressive murine CLL as measured by lymphocyte count and inferior survival. Hemizygous loss of ID4 in nontransformed TCL1-positive B cells enhances cell proliferation triggered by CpG oligonucleotides and decreases sensitivity to dexamethasone-mediated apoptosis. Collectively, this study confirms the importance of the silencing of ID4 in murine and human CLL pathogenesis.
    Type of Publication: Journal article published
    PubMed ID: 21098398
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  • 10
    Keywords: RECEPTOR ; APOPTOSIS ; CANCER ; EXPRESSION ; IN-VIVO ; GENE ; GENE-EXPRESSION ; DIFFERENTIATION ; MECHANISM ; INDUCTION ; CYCLE ; ACID ; DNA methylation ; POLYPHENOLS ; RECEPTORS ; chemoprevention ; histone deacetylase inhibitor ; CHRONIC LYMPHOCYTIC-LEUKEMIA ; HYPERMETHYLATION ; RETINOIC ACID ; HYPOMETHYLATION ; INHIBITORS ; SUPPRESSOR GENES ; HISTONE ACETYLATION ; high-throughput analysis ; CPG-ISLAND METHYLATION ; chemopreventive agents ; TUMOR-SUPPRESSOR GENES ; epigenetic ; histone modifications ; DNA METHYLTRANSFERASE INHIBITORS ; chromatin modifications ; HISTONE METHYLATION ; ABERRANT CRYPT FORMATION ; DNA methyltransferase (DNMT) ; epigenomic ; GREEN TEA POLYPHENOLS ; histone acetyl transferase (HAT) ; histone deacetylase (HDAC) ; NORDIHYDROGUAIARETIC ACID NDGA ; sirtuins ; SMALL-MOLECULE ACTIVATORS
    Abstract: The term "epigenetics" refers to modifications in gene expression caused by heritable, but potentially reversible, changes in DNA methylation and chromatin structure. Given the fact that epigenetic modifications occur early in carcinogenesis and represent potentially initiating events in cancer development, they have been identified as promising new targets for prevention strategies. The present review will give a comprehensive overview of the current literature on chemopreventive agents and their influence on major epigenetic mechanisms, that is DNA methylation, histone acetylation and methylation, and microRNAs, both in vitro and in rodent and human studies, taking into consideration specific mechanisms of action, target sites, concentrations, methods used for analysis, and outcome. Chemopreventive agents with reported mechanisms targeting the epigenome include micronutrients (folate, selenium, retinoic acid, Vit. E), butyrate, polyphenols (from green tea, apples, coffee, and other dietary sources), genistein and soy isoflavones, parthenolide, curcumin, ellagitannin, indol-3-carbinol (I3C) and diindolylmethane (DIM), mahanine, nordihydroguaiaretic acid (NDGA), lycopene, sulfur-containing compounds from Allium and cruciferous vegetables (sulforaphane, phenylethyl isothiocyanate (PEITC), phenylhexyl isothiocyanate (PHI), diallyldisulfide (DADS), allyl mercaptan (AM)), antibiotics (mithramycin A, apicidin), pharmacological agents (celecoxib, DFMO, 5-aza-2'-deoxycytidine and zebularine), compounds affecting sirtuin activity (resveratrol, dihydrocoumarin, cambinol), inhibitors of histone acetyl transferases (anacardic acid, garcinol, ursodeoxycholic acid), and relatively unexplored modulators of histone lysine methylation (chaetocin, polyamine analogues, n-3 polyunsaturated fatty acids). Their effects on global DNA methylation, tumor suppressor genes silenced by promoter methylation, histone modifications, and miRNAs deregulated during carcinogenesis have potential impact on multiple mechanisms relevant for chemoprevention, including signal transduction mediated by nuclear receptors and transcription factors such as NF-kappaB, cell cycle progression, cellular differentiation, apoptosis induction, senescence and others. In vivo studies that demonstrate the functional relevance of epigenetic mechanisms for chemopreventive efficacy are still limited. Future research will need to identify best strategies for chemopreventive intervention, taking into account the importance of epigenetic mechanisms for gene regulation.
    Type of Publication: Journal article published
    PubMed ID: 21158707
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