Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Molecular rules governing de novo methylation in cancer

ABSTRACT: De novo methylation of CpG islands is seen in many tumors, but the general rules governing this process are not known. By analyzing DNA from tumors, as well as normal tissues, and by utilizing a wide range of published data, we have been able to identify a well-defined set of tumor targets, each of which has its own “coefficient” of methylation that is largely determined by its inherent relative ability to recruit the polycomb complex. This pattern is initially formed by a slow process of de novo methylation that occurs during aging and then undergoes expansion early in tumorigenesis, where it may play a role as an inhibitor of development-associated gene activation. We also demonstrate that DNA methylation patterns can be used to diagnose the primary tissue source of tumor metastases.

ORGANISM(S): Homo sapiens

PROVIDER: GSE38142 | GEO | 2014/03/26

SECONDARY ACCESSION(S): PRJNA167279

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Molecular rules governing de novo methylation in cancer

Project description:De novo methylation of CpG islands is seen in many tumors, but the general rules governing this process are not known. By analyzing DNA from tumors, as well as normal tissues, and by utilizing a wide range of published data, we have been able to identify a well-defined set of tumor targets, each of which has its own M-bM-^@M-^\coefficientM-bM-^@M-^] of methylation that is largely determined by its inherent relative ability to recruit the polycomb complex. This pattern is initially formed by a slow process of de novo methylation that occurs during aging and then undergoes expansion early in tumorigenesis, where it may play a role as an inhibitor of development-associated gene activation. We also demonstrate that DNA methylation patterns can be used to diagnose the primary tissue source of tumor metastases. CpG-methylated genomic DNA was enriched using a methyl-DNA immunoprecipitation (mDIP) assay. DNA from the input and bound (enriched) DNA for each sample were labeled and hybridized on the array to define the methylation state of each region.

2014-03-26 | E-GEOD-38142 | biostudies-arrayexpress

Homo sapiens

Project description:Molecular rules governing de novo methylation in cancer

| PRJNA167279 | ENA

Rules governing translation selectivity under limiting ribosome availability

Project description:Rules governing translation selectivity under limiting ribosome availability

| PRJNA513511 | ENA

Rules governing translation selectivity under limiting ribosome availability

Project description:Ribosomopathies are cell-type-specific pathologies related to a ribosomal protein (RP) gene insult. The 5q- syndrome is a somatic ribosomopathy linked to RPS14 gene haploinsufficiency and characterized by a prominent erythroid hypoplasia. Using quantitative proteomic, we show that GATA1 protein expression is low in shRPS14 cells in which ribosome quantities are diminished. Here, we investigated the cause of low GATA1 protein expression in limiting ribosome availability. A global analysis of translation in RPs deficiencies highlights the rules that drive translation selectivity. We demonstrate that in addition of the transcript length, a high codon adaptation index (CAI) and a highly structured 3’UTR are the key characteristics for a selective translation. An integrated analysis of transcriptome and proteome confirms that the post-transcriptional regulations of gene expression are directly linked to the criteria governing the translational selectivity. In particular, these criteria explain GATA1 translation default with unprecedented precision. More generally, the proteins that accumulate along normal erythropoiesis share the determinants of translation selectivity revealed by the conditions of limiting ribosome availability. We performed translatome expression profiling of cells infected with shRPS14 or shSCR

2020-04-28 | GSE124800 | GEO

Default DNA Methylation is Preceded by Broad, Low-Level Transcription in Fetal Male Germ Cells and Is Inversely Patterned by Dynamic H3K4 Methylation (ChIP-chip and MIRA-chip)

Project description:To understand what dictates the emerging patterns of de novo DNA methylation, we mapped DNA methylation, chromatin, and transcription changes in purified fetal mouse germ cells using MIRA-chip, ChIP-chip, and strand-specific RNA-seq, respectively. De novo methylation occurred without any apparent trigger from preexisting repressing chromatin marks but was preceded by broad, low-level transcription along the entire genome in prospermatogonia. Only distinct short sequences remained unmethylated, precisely aligned with constitutive or emerging peaks of H3K4me2. Establishment of methylation at differentially methylated regions (DMRs) of imprinted genes, CpG islands, and IAPs followed these same default rules. Transcription run-through occurred at paternal DMRs with no- or diminishing H3K4me2 peaks. Maternal DMRs remained unmethylated among highly methylated DNA at precisely aligned H3K4me2 peaks with transcription initiating at least in one strand. Our results suggest that the pattern of de novo DNA methylation in prospermatogonia is dictated by opposing actions of broad, low-level transcription and dynamic patterns of active chromatin. ChIP-chip and MIRA-chip were performed to map histone modifications and DNA methylation at different devlopmental time points in germ cells and somatic cells along known imprinted domains and control regions, using custom NimbleGen tiling arrays.

2013-07-31 | E-GEOD-45836 | biostudies-arrayexpress

Default DNA Methylation is Preceded by Broad, Low-Level Transcription in Fetal Male Germ Cells and Is Inversely Patterned by Dynamic H3K4 Methylation (RNA-Seq)

Project description:To understand what dictates the emerging patterns of de novo DNA methylation, we mapped DNA methylation, chromatin, and transcription changes in purified fetal mouse germ cells using MIRA-chip, ChIP-chip, and strand-specific RNA-seq, respectively. De novo methylation occurred without any apparent trigger from preexisting repressing chromatin marks but was preceded by broad, low-level transcription along the entire genome in prospermatogonia. Only distinct short sequences remained unmethylated, precisely aligned with constitutive or emerging peaks of H3K4me2. Establishment of methylation at differentially methylated regions (DMRs) of imprinted genes, CpG islands, and IAPs followed these same default rules. Transcription run-through occurred at paternal DMRs with no- or diminishing H3K4me2 peaks. Maternal DMRs remained unmethylated among highly methylated DNA at precisely aligned H3K4me2 peaks with transcription initiating at least in one strand. Our results suggest that the pattern of de novo DNA methylation in prospermatogonia is dictated by opposing actions of broad, low-level transcription and dynamic patterns of active chromatin. Strand-specific RNA-seq was done in male and female fetal germ cells and somatic gonadal cells at 15.5 dpc to map transcription.

2013-07-31 | E-GEOD-46953 | biostudies-arrayexpress

Default DNA Methylation is Preceded by Broad, Low-Level Transcription in Fetal Male Germ Cells and Is Inversely Patterned by Dynamic H3K4 Methylation (RNA-Seq)

2013-07-31 | GSE46953 | GEO

Default DNA Methylation is Preceded by Broad, Low-Level Transcription in Fetal Male Germ Cells and Is Inversely Patterned by Dynamic H3K4 Methylation (ChIP-chip and MIRA-chip)

2013-07-31 | GSE45836 | GEO

Rules governing selective protein carbonylation.

Project description:BackgroundCarbonyl derivatives are mainly formed by direct metal-catalysed oxidation (MCO) attacks on the amino-acid side chains of proline, arginine, lysine and threonine residues. For reasons unknown, only some proteins are prone to carbonylation.Methodology/principal findingswe used mass spectrometry analysis to identify carbonylated sites in: BSA that had undergone in vitro MCO, and 23 carbonylated proteins in Escherichia coli. The presence of a carbonylated site rendered the neighbouring carbonylatable site more prone to carbonylation. Most carbonylated sites were present within hot spots of carbonylation. These observations led us to suggest rules for identifying sites more prone to carbonylation. We used these rules to design an in silico model (available at http://www.lcb.cnrs-mrs.fr/CSPD/), allowing an effective and accurate prediction of sites and of proteins more prone to carbonylation in the E. coli proteome.Conclusions/significanceWe observed that proteins evolve to either selectively maintain or lose predicted hot spots of carbonylation depending on their biological function. As our predictive model also allows efficient detection of carbonylated proteins in Bacillus subtilis, we believe that our model may be extended to direct MCO attacks in all organisms.

| S-EPMC2751825 | biostudies-literature

Ecological rules governing helminth-microparasite coinfection.

Project description:Coinfection of a host by multiple parasite species has important epidemiological and clinical implications. However, the direction and magnitude of effects vary considerably among systems, and, until now, there has been no general framework within which to explain this variation. Community ecology has great potential for application to such problems in biomedicine. Here, metaanalysis of data from 54 experiments on laboratory mice reveals that basic ecological rules govern the outcome of coinfection across a broad spectrum of parasite taxa. Specifically, resource-based ("bottom-up") and predator-based ("top-down") control mechanisms combined to determine microparasite population size in helminth-coinfected hosts. Coinfection imposed bottom-up control (resulting in decreased microparasite density) when a helminth that causes anemia was paired with a microparasite species that requires host red blood cells. At the same time, coinfection impaired top-down control of microparasites by the immune system: the greater the helminth-induced suppression of the inflammatory cytokine interferon (IFN)-gamma, the greater the increase in microparasite density. These results suggest that microparasite population growth will be most explosive when underlying helminths do not impose resource limitations but do strongly modulate IFN-gamma responses. Surprisingly simple rules and an ecological framework within which to analyze biomedical data thus emerge from analysis of this dataset. Through such an interdisciplinary lens, predicting the outcome of coinfection may become tractable.

| S-EPMC2206576 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data