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At least 91 records · Page 5Linked to original sources
PubMed2006

Modulation of DNA methyltransferase profile by methyl donor starvation followed by gamma irradiation.

DNA methylation is an important epigenetic mechanism of transcriptional control, which plays an essential role in maintaining cellular function. Role of one-carbon transfer agents/methyl donors namely folate, choline and methionine in DNA methylation has been the subject of extensive investigation. The methylation pattern of DNA is established during embryogenesis by DNA methyltransferase 3 (dnmt3) and is subsequently maintained by maintenance methylation activity of the enzyme DNA methyltransferase 1 (dnmt1). Ionizing radiation is known to extensively damage the DNA. Sufficient dietary availability of methyl donors is known to contribute towards one-carbon transfer mediated repair of damaged DNA where folate is involved in nucleotide base synthesis. In the present study, modification in activities of dnmt1 and dnmt3 by methyl donor starvation followed by gamma-irradiation was observed. Assays were based on the catalytic transfer of (3)H-methyl groups from S-adenosyl-L: -methionine to a DNA substrate. Experiments showed a dose and methyl donors starvation dependent attenuation in dnmt1 activity. Attenuation of dnmt1 activity was most significant for diet deprived of all the three-methyl donors. No significant change in nuclear or cytoplasmic dnmt3 activity was observed when either or all the three possible source of dietary methyl group supply were removed. Ionizing radiation and methyl donor deficiency were observed to act synergistically towards inhibiting dnmt1 activity. Present results suggested possibility of interaction among folate, methionine and choline deficiency to potentiate symptoms of ionizing radiation stress. These enzymatic modifications might contribute to altered DNA methylation after chronic feeding of methyl donor free diets followed by gamma irradiation. These results suggested that dietary availability of methyl donors and gamma-radiation stress might significantly alter the dnmt1 profile.

Animals↗
PubMed2025

An Integrated Clinical Genomic and Transcriptomic Subgrouping of Central Chondrosarcoma.

Central conventional chondrosarcoma, a malignant cartilage-producing bone tumor, is the second most common bone sarcoma. Chondrosarcomas are histologically graded, which is so far the best predictor of survival. Early mutations in isocitrate dehydrogenase 1 (IDH1) and IDH2 genes are frequent, leading to the production of the oncometabolite D-2-hydroxyglutarate, which affects DNA methylation, resulting in a preferred chondrogenic differentiation over osteogenic differentiation of mesenchymal stem cells, which are currently considered the precursor cells of chondrosarcoma. DNA methylation profiling has previously revealed distinct profiles between IDH-mutant and IDH-wild-type chondrosarcomas, but the presence of further DNA methylation subgroups indicates that classification based solely on IDH status is too simplistic. In this study, we aim to identify biological subgroups in a total of 116 chondrosarcomas by integrating clinical data, IDH mutation status, gene expression, and genome-wide loss of heterozygosity (LOH). Clinical associations were observed between several factors, including sex and histological grade, as well as tumor site and IDH mutation status. RNA sequencing and genome-wide LOH confirmed the distinction between IDH-wild-type and IDH-mutant chondrosarcomas, where the number of chromosome arms affected by LOH was significantly higher in IDH-wild-type tumors than in IDH-mutant tumors. However, no clear subgroups emerged within each IDH group. Further clustering on RNA expression of differentiation markers identified subgroups characterized by chondrogenic, osteogenic, resting chondrocyte, or dedifferentiated profiles. These different subgroups showed a specific clinical presentation and suggest different precursor cells. Instead of a simple dichotomy between IDH-mutant and IDH-wild-type, our integrated approach highlights interconnected clinical, genomic, and transcriptomic patterns that offer a more nuanced view of chondrosarcoma biology and might potentially guide treatment stratification.

Humans↗
PubMed2025

Blood-based DNA methylation markers for autism spectrum disorder identification using machine learning.

BACKGROUND: Autism spectrum disorder (ASD) is a complex neurodevelopmental disorder lacking objective biomarkers for early diagnosis. DNA methylation is a promising epigenetic marker, and machine learning offers a data-driven classification approach. However, few studies have examined whole-blood, genome-wide DNA methylation profiles for ASD diagnosis in school-aged children. METHODS: We analyzed genome-wide DNA methylation data from GEO dataset GSE113967, including 52 children with ASD and 48 typically developing (TD) controls. Differentially methylated positions (DMPs) were identified, and feature selection was performed using support vector machine-recursive feature elimination with cross-validation (SVM-RFECV). Classification models were developed using random forest (RF), extreme gradient boosting (XGBoost), and decision tree (DT) classifiers. A nomogram visualized feature contributions. RESULTS: A total of 138 DMPs differentiated ASD from TD children. Eleven CpG sites selected by SVM-RFECV formed the basis for model construction. RF and XGBoost achieved the highest accuracy (75%), with DT reaching 70%. Functional annotation indicated enrichment in cell adhesion and immune-related pathways. CONCLUSIONS: This exploratory study demonstrates the feasibility of integrating peripheral blood DNA methylation data with machine learning to distinguish children with ASD. While limited by sample size and moderate accuracy, this study provides methodological insights into the feasibility of integrating epigenetic and computational approaches for ASD-related biomarker exploration.

Humans↗
PubMed2006

The BiSearch web server.

BACKGROUND: A large number of PCR primer-design softwares are available online. However, only very few of them can be used for the design of primers to amplify bisulfite-treated DNA templates, necessary to determine genomic DNA methylation profiles. Indeed, the number of studies on bisulfite-treated templates exponentially increases as determining DNA methylation becomes more important in the diagnosis of cancers. Bisulfite-treated DNA is difficult to amplify since undesired PCR products are often amplified due to the increased sequence redundancy after the chemical conversion. In order to increase the efficiency of PCR primer-design, we have developed BiSearch web server, an online primer-design tool for both bisulfite-treated and native DNA templates. RESULTS: The web tool is composed of a primer-design and an electronic PCR (ePCR) algorithm. The completely reformulated ePCR module detects potential mispriming sites as well as undesired PCR products on both cDNA and native or bisulfite-treated genomic DNA libraries. Due to the new algorithm of the current version, the ePCR module became approximately hundred times faster than the previous one and gave the best performance when compared to other web based tools. This high-speed ePCR analysis made possible the development of the new option of high-throughput primer screening. BiSearch web server can be used for academic researchers at the http://bisearch.enzim.hu site. CONCLUSION: BiSearch web server is a useful tool for primer-design for any DNA template and especially for bisulfite-treated genomes. The ePCR tool for fast detection of mispriming sites and alternative PCR products in cDNA libraries and native or bisulfite-treated genomes are the unique features of the new version of BiSearch software.

DNA Primers↗
PubMed2026

Endothelial cell-specific DNA methylation alterations in breast cancer.

DNA methylation alterations are well-established contributors to carcinogenesis, yet, in the tumor microenvironment (TME), patterns of lineage and cell-specific methylation alterations are not well understood. Single-cell DNA methylation profiling in the TME is limited by technical challenges and high costs. Here, we use bulk DNA methylation, cell type deconvolution (HiTIMED), and an interaction testing framework (CellDMC) to identify reproducible, computationally inferred lineage-specific epigenetic alterations in the TME supported by orthogonal data sources. Tumor endothelial cells (TECs), critical regulators of angiogenesis, vascular permeability, and immune cell trafficking, acquire structural and functional abnormalities that promote tumor growth. We hypothesize that TECs have altered DNA methylation compared with endothelial cells in non-tumor tissues. In genome-scale methylation data from discovery and validation datasets (tumor n = 1071; non-tumor n = 415), we identify and validate >4500 TEC-specific CpGs with altered methylation, many mapping to genes involved in angiogenesis and endothelial function. Integration with gene expression data indicates that TEC-specific methylation alterations may reprogram transcriptional networks controlling angiogenesis. High-resolution, cell lineage-specific epigenetic landscapes can be inferred from bulk methylation data, implicating TEC-specific DNA methylation alterations as potential drivers of cancer angiogenesis and vascular dysfunction and providing a framework for future mechanistic and translational studies of the tumor vasculature.

DNA Methylation↗
PubMed2026

ADCY2 promoter hypomethylation in adolescents with borderline personality disorder: An RRBS study with targeted BSP replication.

BACKGROUND: Borderline Personality Disorder (BPD) is characterized by emotional dysregulation, impulsivity, and interpersonal instability. Although genetic and environmental contributions to BPD have been investigated, epigenetic correlates in adolescents remain poorly understood. The cyclic adenosine monophosphate (cAMP) signaling pathway is implicated in stress responsivity and emotion regulation, but its epigenetic variation in adolescent BPD remains understudied. METHODS: DNA methylation profiling was performed using Reduced Representation Bisulfite Sequencing (RRBS) in buccal epithelial DNA from adolescents with BPD (n = 15) and healthy controls (HC; n = 15). Differentially methylated regions (DMRs) were identified using metilene, a computational tool for detecting DMRs from bisulfite sequencing data, and subjected to Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. Associations between methylation signals and borderline personality features were examined. Adenylate cyclase 2 (ADCY2) promoter methylation was examined using targeted bisulfite sequencing PCR (BSP) in an independent cohort (BPD n = 5; HC n = 5). RESULTS: RRBS identified 7641 DMRs between BPD and HC, with enrichment in pathways related to neuronal signaling and synaptic organization. A hypomethylated DMR was detected in the ADCY2 promoter, a gene implicated in cAMP signaling. Lower ADCY2 promoter methylation was associated with greater clinical severity, including emotional dysregulation, borderline traits, anxiety symptoms, and self-injury behaviors (r=-0.71 to -0.83; all p < 0.0001). Hypomethylation of the ADCY2 promoter was replicated in the independent cohort. CONCLUSIONS: This exploratory two-stage epigenetic study suggests that ADCY2 promoter hypomethylation in peripheral buccal epithelial DNA is associated with core symptom dimensions of adolescent BPD. These findings support a role for cAMP-related epigenetic variation in BPD and warrant replication in longitudinal studies.

ADCY2↗
PubMed1996

Cytosine methylation: quantitation by automated genomic sequencing and GENESCAN analysis.

Bisulfite treatment and PCR amplification of genomic DNA permits the methylation analysis of any cytosine residue in a target sequence. By cloning and sequencing the PCR product, the methylation of individual molecules can be determined, whereas direct sequencing of the PCR product can provide an average of the methylation status in the population of molecules. Reliable quantitation of cytosine methylation by direct sequencing, however, has not been possible with current methods. In this paper we describe an accurate and innovative protocol to directly quantitate the methylation of any cytosine residue in the target sequence by fluorescence-based automated genomic sequencing. Only the cytosine and thymine residues of bisulfite-treated and amplified genomic DNA are sequenced. The degree of methylation is obtained by direct comparison of the cytosine and thymine signals, which have been labeled with the same fluorescent dyes. GENESCAN analysis is employed to achieve a fast and accurate estimate of methylation at every cytosine in the target sequence. Combining direct bisulfite genomic sequencing and GENESCAN analysis permits the rapid survey of detailed DNA methylation profiles. Using this approach we have found the unexpected result that multicopy plasmid DNA grown in a Dcm host is not always fully methylated as suggested by restriction enzyme data.

Autoanalysis↗
PubMed2004

A comparison of cluster analysis methods using DNA methylation data.

MOTIVATION: Aberrant DNA methylation is common in cancer. DNA methylation profiles differ between tumor types and subtypes and provide a powerful diagnostic tool for identifying clusters of samples and/or genes. DNA methylation data obtained with the quantitative, highly sensitive MethyLight technology is not normally distributed; it frequently contains an excess of zeros. Established tools to analyze this type of data do not exist. Here, we evaluate a variety of methods for cluster analysis to determine which is most reliable. RESULTS: We introduce a Bernoulli-lognormal mixture model for clustering DNA methylation data obtained using MethyLight. We model the outcomes using a two-part distribution having discrete and continuous components. It is compared with standard cluster analysis approaches for continuous data and for discrete data. In a simulation study, we find that the two-part model has the lowest classification error rate for mixture outcome data compared with other approaches. The methods are illustrated using DNA methylation data from a study of lung cancer cell lines. Compared with competing hierarchical clustering methods, the mixture model approaches have the lowest cross-validation error for detecting lung cancer subtype (non-small versus small cell). The Bernoulli-lognormal mixture assigns observations to subgroups with the lowest uncertainty. AVAILABILITY: Software is available upon request from the authors. SUPPLEMENTARY INFORMATION: http://www-rcf.usc.edu/~kims/SupplementaryInfo.html

Algorithms↗
PubMed2005

DNA methylation in promoter regions of red cell membrane protein genes in healthy individuals and patients with hereditary membrane disorders.

The methylation state of 5'-CG-3' sites is known to be linked to the regulation of promoter function by modulating DNA-protein interactions and to the structure of chromatin. As part of a project to determine methylation patterns in the human genome, we examined the methylation profiles of several genes for human erythroid membrane proteins: ELB42 (protein 4.2), EPB3 (band 3), SPTB gene (beta-spectrin), and ANK1 (ankyrin). The bisulfite protocol of the genomic sequencing method was applied. The number of 5'-CG-3' dinucleotides was the most abundant in SPTB and ANK1, much less in EPB3, and the least in ELB42. In the DNA of peripheral blood mononuclear cells from healthy individuals, the promoter regions of EPB3 and ELB42 were extensively methylated, but the SPTB and ANK1 promoters were totally unmethylated. We also investigated methylation profiles in peripheral blood mononuclear cells from patients with red cell membrane diseases, such as complete protein 4.2 deficiency due to ELB42 mutations, hereditary spherocytosis with EPB3 mutations, and hereditary elliptocytosis with SPTB mutations. The DNA methylation states in these genes of erythroid cells, which we obtained at the second phase of the 2-phase liquid culture of erythroid precursor cells in the peripheral blood, were essentially identical or very similar to those of peripheral blood mononuclear cells. In disease states, the DNA methylation profiles of these red cell membrane protein genes were essentially not different from those in healthy individuals (statistically not significant).

Anemia↗
PubMed2004

DNA-methylation alterations and exchanges during in vitro cellular differentiation in rose (Rosa hybrida L.).

DNA-methylation profiles of leaf tissues of Rosa hybrida cv. Carefree Beauty collected from in vivo-grown greenhouse plants, in vitro-grown proliferating shoots at different passages, regenerants of embryogenic callus, regenerants of organogenic callus, as well as calli from undifferentiated callus (UC), embryogenic callus, and organogenic callus were investigated using an amplified fragment-length polymorphism (AFLP)-based detection technique. Three types of AFLP bands were recovered. Type I bands were observed with both isoschizomers Msp and HpaII, while type II and type III bands were observed only with MspI and HpaII, respectively. Sequence analysis of the three types of AFLP bands revealed that a nonmethylated MspI/HpaII-recognition site 5'-CCGG-3' resulted in a type I band, while an inner 5-methylcytosine generated most type II and type III bands. About 40% of inner and 20% of outer cytosines in 5'-CCGG-3' sequences were fully methylated, and only a few hemimethylated outer cytosines were observed. Changes in types of AFLP bands among different tissues were frequently observed, including appearance and disappearance of type I, II, and III AFLP bands, as well as exchanges between either type I and type II or type I and type III AFLP bands. Methylation alterations of outer cytosines in 5'-CCGG-3' sequences triggered appearance and disappearance of type I and II AFLP bands. Methylation changes of both outer and inner cytosines resulted in either removal or generation of type III AFLP bands. Methylation alteration of an inner cytosine was responsible for exchange between type I and type II, while hemimethylation of an outer cytosine accounted for exchange between type I and type III AFLP bands. During UC induction, a significant DNA-methylation alteration was detected in both inner and outer cytosines. Variations in methylation profiles significantly differed between somatic embryogenesis and in vitro organogenesis. Demethylation of outer cytosines occurred at a high frequency during somatic embryogenesis, and most altered AFLP bands in embryogenic callus were passed on to its regenerants. However, most methylation-altered AFLP bands during organogenesis were recovered in shoot regenerants derived via organogenic callus. Seven tissue-specific bands were isolated, cloned, and sequenced. Blast search revealed that two of these might be derived from functional genes.

Amino Acid Sequence↗
PubMed2006

Expression of DNMT-1 in patients with atopic dermatitis.

DNA methylation is known to play an important role in gene transcription and alterations of methylation that contribute to the development of certain disorders such as cancer, immunodeficiency, and autoimmune diseases. We investigated the DNA methylation profiles in patients with atopic dermatitis (AD). Messenger RNA (mRNA) levels for DNA methyltransferase-1 (DNMT-1) in peripheral blood mononuclear cells (PBMC) were examined using a real-time quantitative polymerase chain reaction method. The levels of DNMT-1 mRNA were significantly lower in PBMC from the AD patients who had higher serum IgE levels compared with normal controls. Our observations suggest that suppression of DNMT-1 might be related to the pathogenesis of AD, especially in whom serum IgE level is high. This is the first report of DNMT-1 expression in AD patients.

Adolescent↗
PubMed2026

A murine model of sepsis induces age- and sex-specific chromatin remodeling in myeloid-derived suppressor cells.

INTRODUCTION: Sepsis survivors frequently develop long-term immune dysfunction, but the epigenetic mechanisms underlying persistent myeloid suppression remain unclear. Myeloid-derived suppressor cells (MDSCs), whose function is shaped by host age and sex, are key contributors to post-sepsis immune dysregulation. METHODS: Here, we present a high-resolution epigenetic map targeting gene promoters of MDSCs after sepsis and daily chronic stress using MAPit-FENGC, a single-molecule assay that simultaneously profiles DNA methylation and chromatin accessibility. In a clinically relevant murine model, including young and older adult male and female mice, splenic MDSCs were isolated for MAPit-FENGC and single-cell RNA sequencing. RESULTS: Unsupervised clustering identified nine promoter classes reflecting chromatin dynamics: age- and sex-dependent sepsis-induced opening (Classes 1-4), persistent closure with varying levels of DNA methylation (Classes 5-7), and constitutive openness post-sepsis (Classes 8, 9). Transcriptomic profiling corroborated these promoter states, linking accessibility with gene expression. CONCLUSIONS: These findings define promoter-level epigenetic classes across a targeted locus panel in splenic CD11b+Gr1+ cells within this murine sepsis model and generate mechanistic hypotheses regarding age- and sex-associated chromatin states.

Animals↗
PubMed2005

[Applications of DNA methylation markers in forensic medicine].

DNA methylation is a post-replication modification that is predominantly found in cytosines of the dinucleotide sequence CpG. Epigenetic information is stored in the distribution of the modified base 5-methylcytosine. DNA methylation profiles represent a more chemically and biologically stable source of molecular diagnostic information than RNA or most proteins. Recent advances attest to the great promise of DNA methylation markers as powerful future tools in the clinic. In the past decade, DNA methylation analysis has been revolutionized by two technological advances--bisulphite modification of DNA and methylation-specific polymerase chain reaction (MSP). The methylation pattern of human genome is space-time specific, sex-specific, parent-of-origin specific and disease specific, providing us an alternative way to solve forensic problems.

Base Sequence↗
PubMed2002

Alterations of DNA methylation in hematologic malignancies.

The DNA methylation profile of cancer cells is frequently characterized by global hypomethylation and simultaneous hypermethylation of selected CpG island gene promoters. In recent years, the epigenetic phenomenon of DNA promoter methylation has gained increasing recognition as an important mechanism for transcriptional inactivation of cancer related genes. Studies on both liquid and solid tumors have revealed myriad aberrant methylation events, some of which may provide important clues to the pathogenesis of these tumors. The identification of these methylation alterations and elucidation of the mechanistic events surrounding them are of prime importance, as the methylation status of cancer cells can now be manipulated in vivo with demethylating chemotherapeutics.

Cell Transformation, Neoplastic↗
PubMed2004

Evidence that general genomic hypomethylation and focal hypermethylation are two independent molecular events of non-Hodgkin's lymphoma.

Changes in the DNA methylation profile, including general genomic hypomethylation and regional hypermethylation, have been shown to coexist in many neoplastic tissues. However, the relationship between, and significance of, these different forms of DNA methylation dysregulation in disease onset, progression, or maintenance remains unclear. Previously, our work has shown that the CpG dinucleotide-rich gene Myf-3 is hypermethylated in most cases of malignant lymphoproliferative disease (LPD). However, it is unknown whether malignant transformation of lymphoid cells is associated with general genomic hypomethylation and whether regional hypermethylation is restricted to CpG islands. The relationship between the status of general genomic methylation and the methylation of CpG and non-CpG islands can be clearly investigated in DNA from tumors of patients suffering malignant LPD, as monoclonalilty of malignant cells in LPD can be readily confirmed. In this study, the relationships between the methylation status of a region of the PAX7 paired box, which is not contained within a CpG island, general genomic hypomethylation, and the methylation status of Myf-3 was examined in 24 cases of LPD. Results revealed that hypermethylation of the PAX7 paired box is strongly associated with hypermethylation of Mvf-3, indicating the abnormal hypermethylating activity in malignant lymphoid cells does not specifically target CpG islands. Further, general genomic hypomethylation was shown to be associated with malignant LPD but not with regional hypermethylation, indicating that the mechanisms responsible for the generation of each of these disturbed DNA methylation phenotypes act independently as one of a number of permissive but not essential steps in the malignant transformation of lymphoid cells.

Case-Control Studies↗
PubMed2006

Epigenomics: mapping the methylome.

DNA methylation is integral to normal development and disease processes. However, the genomic distribution of methylated sequences--the methylome--is poorly understood. We have recently developed a platform technology for rapid assessment of methylation status throughout the human genome in a high-resolution, high-throughput manner. This is achieved by coupling a methylated DNA immunoprecipitation (MeDIP) method for isolating methyl cytosine rich fragments with array-based comparative genomic hybridization (array CGH). Using a combination of whole genome tiling path BAC arrays and CpG island microarrays, DNA methylation profiles are obtained simultaneously at both genome-wide and locus-specific levels. A comparison between male and female DNA using MeDIP-array CGH revealed unexpected hypomethylation of the inactive x-chromosome in gene-poor regions. Furthermore, comparisons between cancer and noncancer cell types yielded differential methylation patterns that link genetic and epigenetic instability offering a new approach to decipher misregulation in cancer. Finally, we provide new data showing epigenomic instability in lung cancer cells with concurrent regions of genetic and epigenetic alterations harboring known oncogenes.

Chromatin Immunoprecipitation↗
PubMed2025

DNA Methylation-Based Classification of Kidney Neoplasms.

Renal neoplasms are morphologically and molecularly heterogeneous, with their diagnosis often hindered by interobserver variability and overlapping microscopic features. A subset of cases is unclassifiable despite immunohistochemical, mutation, and cytogenetic-based diagnostic workup. Through examination of the genome-wide DNA methylation signatures of over 2000 renal neoplasms, we identified 23 coherent groups that correlate with known neoplasm types and identified novel clinically relevant subtypes of existing neoplasm types. We used machine learning models to develop and validate a classifier trained on DNA methylation profiles of 1284 samples. The classifier was tested on an external data set of 287 renal neoplasms with >90% concordance between expected neoplasm type and high-score DNA methylation-based classification. Discordance between the original histologic label and methylation class led to potential reclassification of some cases. This work demonstrates proof of principle for the feasibility of a DNA methylation classifier as a clinically useful tool to assist in the diagnosis of renal neoplasms.

Humans↗
PubMed2007

Genome-wide and locus-specific DNA hypomethylation in G9a deficient mouse embryonic stem cells.

In the mammalian genome, numerous CpG-rich loci define tissue-dependent and differentially methylated regions (T-DMRs). Euchromatin from different cell types differs in terms of its tissue-specific DNA methylation profile as defined by these T-DMRs. G9a is a euchromatin-localized histone methyltransferase (HMT) and catalyzes methylation of histone H3 at lysines 9 and 27 (H3-K9 and -K27). To test whether HMT activity influences euchromatic cytosine methylation, we analyzed the DNA methylation status of approximately 2000 CpG-rich loci, which are predicted in silico, in G9a(-/-) embryonic stem cells by restriction landmark genomic scanning (RLGS). While the RLGS profile of wild-type cells contained about 1300 spots, 32 new spots indicating DNA demethylation were seen in the profile of G9a(-/-) cells. Virtual-image RLGS (Vi-RLGS) allowed us to identify the genomic source of ten of these spots. These were confirmed to be cytosine demethylated, not just at the Not I site detected by the RLGS but extending over several kilobase pairs in cis. Chromatin immunoprecipitation (ChIP) confirmed these loci to be targets of G9a, with decreased H3-K9 and/or -K27 dimethylation in the G9a(-/-) cells. These data indicate that G9a site-selectively contributes to DNA methylation.

Animals↗