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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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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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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

2013-10-10 | E-GEOD-45342 | biostudies-arrayexpress

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2014-03-28 | E-GEOD-56310 | biostudies-arrayexpress

Aberrant DNA methylation in rhabdomyosarcoma

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

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