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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Genome wide DNA methylation analysis of leukemia and reprogrammed leukemia cells

ABSTRACT: This SuperSeries is composed of the following subset Series: GSE33226: Genome wide DNA methylation analysis of leukemia and reprogrammed leukemia cells (gene expression) GSE33230: Genome wide DNA methylation analysis of leukemia and reprogrammed leukemia cells (sequencing) Refer to individual Series

ORGANISM(S): Homo sapiens

SUBMITTER: Touati Benoukraf

PROVIDER: E-GEOD-33231 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Genome wide DNA methylation analysis of leukemia and reprogrammed leukemia cells (sequencing)

Project description:We analyzed the methylation pattern of a well characterized leukemia cell line, named K562. Furthermore, we decided to investigate how the malignant epiegenome change during the reprogramming process We used RRBS analysis to investigate the methylation pattern in leukemia and reprogrammed leukemia (LiPS).We show that the erasure of the epigenetic aberrancies have functional consequences on leukemia phenotype

2012-10-01 | E-GEOD-33230 | biostudies-arrayexpress

Genome wide DNA methylation analysis of leukemia and reprogrammed leukemia cells

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RRBS (Reduced Representation Bisulfite Sequencing) of HL60

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2012-12-01 | E-GEOD-32168 | biostudies-arrayexpress

Relationship between DNMT1-RNA interactions, DNA methylation and gene expression

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

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Differential methylation between mouse embyronic stem cell states

Project description:We generated RRBS data between Rex1-high and Rex1-low cells to identify differentially methylated promoters. We observe bimodal methylation levels in both subpopulations, and that Rex1-low cells accumulate increased levels of methylation, frequently as a function of local CpG density We sorted Rex1 high and low cells using a GFP-knockin reporter cell line (kindly provided by Austin Smith), and performed RRBS on the subpopulations

2014-07-21 | E-GEOD-58396 | biostudies-arrayexpress

Fundamental differences in promoter CpG island DNA hypermethylation between human cancer and genetically engineered mouse models of cancer [RRBS]

Project description:Genetic and epigenetic alterations are essential for the initiation and progression of human cancer. We previously reported that primary human medulloblastomas showed extensive cancer-specific CpG island DNA hypermethylation in critical developmental pathways. To determine whether genetically engineered mouse models (GEMMs) of medulloblastoma have comparable epigenetic changes, we assessed genome-wide DNA methylation in three mouse models of medulloblastoma. In contrast to human samples, very few loci with cancer-specific DNA hypermethylation were detected, and in almost all cases the degree of methylation was relatively modest compared to the dense hypermethylation in the human cancers. To determine if this finding was common to other GEMMs, we examined a Burkitt lymphoma and breast cancer model and did not detect promoter CpG island DNA hypermethylation, suggesting that human cancers and at least some GEMMs are fundamentally different with respect to this epigenetic modification. These findings provide an opportunity to both better understand the mechanism of aberrant DNA methylation in human cancer and construct better GEMMs to serve as preclinical platforms for therapy development. Examination of DNA methylation in one representative human medulloblastoma patient sample and three different mouse models of medulloblastoma using RRBS

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Transient expression of Bcl6 is sufficient for oncogenic function and induction of mature B-cell lymphoma

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Fundamental differences in promoter CpG island DNA hypermethylation between human cancer and genetically engineered mouse models of cancer

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

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Project description:Many pediatric malignancies are embryonal in nature, and one hypothesis for the origin of embryonal tumors is that they arise from a defect in differentiation, either by an inability to terminally differentiate or a reversion to a pluripotent state. There is emerging evidence that epigenetic regulation plays an important role in the transition from embryonic stem cell to a more committed cell fate, utilizing both de novo DNA methylation and poised M-bM-^@M-^XbivalentM-bM-^@M-^Y chromatin domains (H3K27me3 and H3K4me3) to abolish pluripotency and gain lineage- and cell-type-specific characteristics as a cell differentiates. Thus inappropriate epigenetic silencing by aberrant DNA methylation of bivalent genes required for differentiation could lead to the uncontrolled cell growth observed in cancer. Our broad hypothesis is that aberrant DNA methylation in cancer is targeted to a non-random subset of critical pathways used in normal development. This dysregulation of the normal epigenetic program used in development promotes cellular proliferation and provides a mechanism to block differentiation in pediatric cancers, such as rhabdomyosarcoma. Examination of DNA methylation in fourteen human rhabdomyosarcoma patient samples using RRBS. In addition, RRBS was used to examine DNA methylation in one human rhabdomyosarcoma cell line (RD) forced to terminally differentiate by expression of the forced heterodimer MyoD~E12 (MDE). Lastly, RRBS was used to examine DNA methylation changes during normal differentiation in one primary human normal myoblast cell line

2014-10-22 | E-GEOD-61150 | biostudies-arrayexpress

Genome wide DNA methylation of Epstein-Barr virus infected immortalized normal oral keratinocytes

Project description:The oral cavity is the persistent reservoir for EBV with lifelong infection of resident epithelial and B cells. Infection of these cell types results in distinct EBV gene expression patterns that are regulated by epigenetic modifications involving DNA methylation and chromatin structure. Such regulation of EBV gene expression relies on viral manipulation of the host epigenetic machinery that may inadvertently result in long-lasting, oncogenic host epigenetic reprogramming. To test this hypothesis in the context of EBV infection of epithelial cells, we established a transient infection model to identify the epigenetic consequences after EBV infection of immortalized normal oral keratinocytes and subsequent viral loss. NOK cells were single cell cloned (designated as cl1) and EBV infected by co-culture with a recombinant Akata EBV strain carrying neomcycin resistance and GFP expression cassette in place of EBV BXLF1. Cells were selected with 350 ug/ml G418. As a selection control, cells were transfected a plasmid carrying a neomycin resistance cassette. Cells were passaged 10 times with G418, followed by removal of selection pressure. After an additional 10 passages, cells were single cell cloned and the presence of EBV was determined by various methods. Three clones were identified as being EBV negative and said to be transiently infected. Uninfected parental and vector transfected cells were passaged in the same manner and also single cell cloned. The DNA methylation profiles were examined using reduced representation bisulfite sequencing.

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