GEO DataSets

(Submitter supplied) To examine the global impact of iAs on DNA methylation patterns. Genomic DNA was Bisulfite converted and analyzed using Mini methly-seq.

Organism:

Homo sapiens

Type:

Methylation profiling by high throughput sequencing

Platforms:

GPL11154 GPL18460

4 Samples

Download data: BIGBED

(Submitter supplied) Chronic low dose inorganic arsenic (iAs) exposure leads to changes in gene expression and epithelial-to-mesenchymal transformation. During this transformation, cells adopt a fibroblast-like phenotype accompanied by profound gene expression changes. While many mechanisms have been implicated in this transformation, studies that focus on the role of epigenetic alterations in this process are just emerging. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platforms:

GPL17585 GPL17586

8 Samples

Download data: CEL, CHP

(Submitter supplied) To examine the global impact of iAs on DNA hdroxymethylation patterns. Genomic DNA was glucosylated, digested and analyzed using Reduced Representation Hydroxymethylation Profiling.

Organism:

Homo sapiens

Type:

Methylation profiling by high throughput sequencing

Platform:

GPL11154

2 Samples

Download data: BIGBED

(Submitter supplied) Arsenic (As) exposure is a significant worldwide environmental health concern. Low dose, chronic arsenic exposure has been associated with higher risk of skin, lung, and bladder cancer, as well as cardiovascular disease and diabetes. While arsenic-induced biological changes play a role in disease pathology, little is known about the dynamic cellular changes due to arsenic exposure and withdrawal. In these studies, we seek to understand the molecular mechanisms behind the biological changes induced by chronic low doses of arsenic exposure. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL17586

8 Samples

Download data: CEL

(Submitter supplied) The faithful inheritance of the epigenome is critical for cells to maintain gene expression programs and cellular identity across cell divisions. We mapped strand-specific DNA methylation after replication forks and show maintenance of the vast majority of the DNA methylome within 20 minutes of replication and inheritance of some hemimethylated CpG dinucleotides (hemiCpGs). Mapping the nascent DNA methylome targeted by each of the three DNA methyltransferases (DNMTs) reveals interactions between DNMTs and substrate daughter cytosines en route to maintenance methylation or hemimethylation. more...

Organism:

Homo sapiens; Mus musculus

Type:

Methylation profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing; Other

Platforms:

GPL16791 GPL17021

53 Samples

Download data

(Submitter supplied) There is strong epidemiologic evidence supporting that exposure to inorganic arsenic (iAs) exposure is responsible for a myriad of adverse health effects, including carcinogenesis of the bladder. This research aimed to identify novel epigenetic biomarkers of iAs exposure in target cells within a human population. Here we assessed genome-wide, gene-specific promoter DNA methylation levels assessed in exfoliated human bladder uroepithelial cells (BECs) in relationship to BEC iAs, monomethylated As (MMAs), dimethylated As (DMAs), and total As (tAs) concentrations from 46 individuals with varying levels of As exposure in Chihuahua, Mexico. more...

Organism:

Homo sapiens

Type:

Methylation profiling by genome tiling array

Platform:

GPL5082

46 Samples

Download data: CEL, TXT

(Submitter supplied) We define how chronic cigarette smoke-induced time-dependent epigenetic alterations can sensitize human bronchial epithelial cells (HBEC) for transformation by a single oncogene. The smoke-induced, chromatin changes include initial repressive polycomb marking of genes later manifesting abnormal DNA methylation by 10 months. At this time, cells manifest epithelial to mesenchymal changes, anchorage-independent growth and upregulated RAS/MAPK signaling with silencing of hyper-methylated genes normally inhibiting these pathways and which are associated with smoking related NSCLC. more...

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL16791

20 Samples

Download data: BED

(Submitter supplied) We define how chronic cigarette smoke-induced time-dependent epigenetic alterations can sensitize human bronchial epithelial cells (HBEC) for transformation by a single oncogene. The smoke-induced, chromatin changes include initial repressive polycomb marking of genes later manifesting abnormal DNA methylation by 10 months. At this time, cells manifest epithelial to mesenchymal changes, anchorage-independent growth and upregulated RAS/MAPK signaling with silencing of hyper-methylated genes normally inhibiting these pathways and which are associated with smoking related NSCLC. more...

Organism:

Homo sapiens

Type:

Other

Platforms:

GPL15520 GPL16791

10 Samples

Download data

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Homo sapiens

Type:

Methylation profiling by genome tiling array; Expression profiling by array; Other; Genome binding/occupancy profiling by high throughput sequencing

4 related Platforms

86 Samples

Download data: BED, IDAT, PDF, TXT

(Submitter supplied) We define how chronic cigarette smoke-induced time-dependent epigenetic alterations can sensitize human bronchial epithelial cells (HBEC) for transformation by a single oncogene. The smoke-induced, chromatin changes include initial repressive polycomb marking of genes later manifesting abnormal DNA methylation by 10 months. At this time, cells manifest epithelial to mesenchymal changes, anchorage-independent growth and upregulated RAS/MAPK signaling with silencing of hyper-methylated genes normally inhibiting these pathways and which are associated with smoking related NSCLC. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL10332

16 Samples

Download data: PDF, TXT

(Submitter supplied) We define how chronic cigarette smoke-induced time-dependent epigenetic alterations can sensitize human bronchial epithelial cells (HBEC) for transformation by a single oncogene. The smoke-induced, chromatin changes include initial repressive polycomb marking of genes later manifesting abnormal DNA methylation by 10 months. At this time, cells manifest epithelial to mesenchymal changes, anchorage-independent growth and upregulated RAS/MAPK signaling with silencing of hyper-methylated genes normally inhibiting these pathways and which are associated with smoking related NSCLC. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL10332

9 Samples

Download data: PDF, TXT

(Submitter supplied) We define how chronic cigarette smoke-induced time-dependent epigenetic alterations can sensitize human bronchial epithelial cells (HBEC) for transformation by a single oncogene. The smoke-induced, chromatin changes include initial repressive polycomb marking of genes later manifesting abnormal DNA methylation by 10 months. At this time, cells manifest epithelial to mesenchymal changes, anchorage-independent growth and upregulated RAS/MAPK signaling with silencing of hyper-methylated genes normally inhibiting these pathways and which are associated with smoking related NSCLC. more...

Organism:

Homo sapiens

Type:

Methylation profiling by genome tiling array

Platform:

GPL13534

31 Samples

Download data: IDAT, TXT

(Submitter supplied) Genome-wide DNA methylation profiles of TGF-beta ovarian cancer cells were obtained using next generation Illumina Infinium 450k assay which includes over 450,000 GpG sites.

Organism:

Homo sapiens

Type:

Methylation profiling by genome tiling array

Platform:

GPL13534

12 Samples

Download data: TXT

(Submitter supplied) Genome-wide CpG-island methylation profiling on pediatric AML samples was performed to identify specific methylation patterns discriminating particular AML subgroups from the rest of AML samples based on the methylation profile.

Organism:

Homo sapiens

Type:

Methylation profiling by genome tiling array

Platform:

GPL9767

152 Samples

Download data: TXT

(Submitter supplied) Aberrant DNA hypermethylation of promoter CpG islands in the context of a hypomethylated genome is a hallmark of cancer. Thus far there is no human experimental model available to mechanistically investigate this phenomenon. Here we show that upon reprogramming of human embryonic stem cells to the naïve state, the acquisition of a globally hypomethylated genome is accompanied by hypermethylation of a subset of bivalent promoter CpG islands, resulting in a DNA methylome comparable to the human inner cell mass. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL18573

15 Samples

Download data: TXT

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Homo sapiens

Type:

Methylation profiling by genome tiling array; Expression profiling by high throughput sequencing

Platforms:

GPL21145 GPL18573

54 Samples

Download data: IDAT

(Submitter supplied) Aberrant DNA hypermethylation of promoter CpG islands in the context of a hypomethylated genome is a hallmark of cancer. Thus far there is no human experimental model available to mechanistically investigate this phenomenon. Here we show that upon reprogramming of human embryonic stem cells to the naïve state, the acquisition of a globally hypomethylated genome is accompanied by hypermethylation of a subset of bivalent promoter CpG islands, resulting in a DNA methylome comparable to the human inner cell mass. more...

Organism:

Homo sapiens

Type:

Methylation profiling by genome tiling array

Platform:

GPL21145

8 Samples

Download data: IDAT, TXT

(Submitter supplied) Aberrant DNA hypermethylation of promoter CpG islands in the context of a hypomethylated genome is a hallmark of cancer. Thus far there is no human experimental model available to mechanistically investigate this phenomenon. Here we show that upon reprogramming of human embryonic stem cells to the naïve state, the acquisition of a globally hypomethylated genome is accompanied by hypermethylation of a subset of bivalent promoter CpG islands, resulting in a DNA methylome comparable to the human inner cell mass. more...

Organism:

Homo sapiens

Type:

Methylation profiling by genome tiling array

Platform:

GPL21145

8 Samples

Download data: IDAT, TXT

(Submitter supplied) Aberrant DNA hypermethylation of promoter CpG islands in the context of a hypomethylated genome is a hallmark of cancer. Thus far there is no human experimental model available to mechanistically investigate this phenomenon. Here we show that upon reprogramming of human embryonic stem cells to the naïve state, the acquisition of a globally hypomethylated genome is accompanied by hypermethylation of a subset of bivalent promoter CpG islands, resulting in a DNA methylome comparable to the human inner cell mass. more...

Organism:

Homo sapiens

Type:

Methylation profiling by genome tiling array

Platform:

GPL21145

15 Samples

Download data: IDAT, TXT

(Submitter supplied) Aberrant DNA hypermethylation of promoter CpG islands in the context of a hypomethylated genome is a hallmark of cancer. Thus far there is no human experimental model available to mechanistically investigate this phenomenon. Here we show that upon reprogramming of human embryonic stem cells to the naïve state, the acquisition of a globally hypomethylated genome is accompanied by hypermethylation of a subset of bivalent promoter CpG islands, resulting in a DNA methylome comparable to the human inner cell mass. more...

Organism:

Homo sapiens

Type:

Methylation profiling by genome tiling array

Platform:

GPL21145

8 Samples

Download data: IDAT, TXT