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DNA methylation profiling upon treatment with NTX-301 or decitabine in AML cells

ABSTRACT: DNA methylation profiling upon treatment with NTX-301 or decitabine in AML cells

PROVIDER: PRJNA777433 | ENA |

REPOSITORIES: ENA

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DNA methylation profiling upon treatment with NTX-301 or decitabine in AML cells

Project description:A novel hypomethylating agent NTX-301 is a promising therapeutic agent for AML patients. To examine its mechanisms of action, we produced methylome data upon treatment with NTX-301 or decitabine (DAC) in MV4-11 cell line.

2022-11-30 | GSE187291 | GEO

Gene expression profiling upon treatment with NTX-301

Project description:A novel hypomethylating agent NTX-301 is a promising therapeutic agent for AML patients. To examine its mechanisms of action, we produced gene expression data upon treatment with NTX-301 or decitabine (DAC) in AML cell lines.

2022-04-20 | GSE188392 | GEO

Gene expression profiling upon treatment with NTX-301 in MV4-11

2022-04-20 | GSE187285 | GEO

Decitabine alters DNA methylation in AML patients

Project description:Sequential assessment of global mRNA expression in myeloblasts isolated from peripheral blood of eight AML patients treated with Decitabine within a phase II study (trial 00331). Total RNA was isolated after enrichment of peripheral blood myeloblasts directly before and directly after (median day 3) Decitabine administration

2012-12-12 | E-MEXP-3737 | biostudies-arrayexpress

Transient low-dose decitabine treatment of primary AML samples

Project description:Genome-wide DNA methylation profiling of primary AML samples treated with 100nM decitabine (DAC), cytarabine (AraC), or DMSO. Eight distinct AML samples were grown using an in vitro stromal co-culture system for 4 days and then treated with either DAC, Ara-C or DMSO for 3 days. DNA was prepared for genome-wide methylation analysis with the Illumina Infinium 450k Human DNA methylation BeadChip. DNA from each sample/treatment was analyzed on duplicate arrays. Bisulfite-converted DNA from 24 samples was hybridised to the Illumina Infinium 450k Human Methylation Beadchip in duplicate (replicates are indicated by array plate number).

2012-12-18 | E-GEOD-40870 | biostudies-arrayexpress

Gene expression profiling in primary AML cells treated with decitabine and cytarabine

Project description:Acute myeloid leukemia (AML), and other myeloid malignancies, are frequently treated with hypomethylating agents like decitabine. Alterations in the epigenome, induced by decitabine, are likely to result in gene expression changes. The effects of decitabine have not been systemically studied using primary AML samples. We cultured 18 different primary AML samples for 7 days, the last 3 days of which included 100 nM decitabine (DAC) or 100 nm cytarabine (AraC). We hypothesized that decitabine treatment would result in detectable and consistent gene expression changes. For comparison, we also analyzed mRNA from cells treated with DMSO control (mock) and mRNA from uncultured cells taken at the time of diagnosis.

2012-12-18 | E-GEOD-40442 | biostudies-arrayexpress

Gene expression profiling upon treatment with NTX-301

Project description:Gene expression profiling upon treatment with NTX-301

| PRJNA778722 | ENA

Transient low-dose decitabine treatment of primary AML samples

2012-12-18 | GSE40870 | GEO

Gene expression profiling in primary AML cells treated with decitabine and cytarabine

2012-12-18 | GSE40442 | GEO

CpG methylation patterns and decitabine treatment response in acute myeloid leukemia cells and normal hematopoietic precursors

Project description:The DNA hypomethylating drug decitabine maintains normal hematopoietic stem and progenitor cell (HSPC) self-renewal but induces terminal differentiation in acute myeloid leukemia (AML) cells. To better understand the basis for this contrasting treatment effect, the baseline expression of key lineage-specifying transcription factor (TF) (eg., CEBPa) and key late differentiation TF (CEBPe), was examined in normal, myelodysplastic (MDS) and AML primary cells and cell lines. To appreciate the role of differentiation in hypomethylation of some CpG by decitabine treatment but not others, promoter CpGs, analyzed by microarray and mass spectrometry, were categorized by the direction of methylation change during normal myeloid differentiation. In MDS/AML cells, high expression of CEBPa, relatively low expression of CEBPe (a gene target of CEBPa), hypermethylation of CEBPe promoter CpG, and the methylation pattern at differentiation sensitive promoter CpGs analyzed by microarray, suggested lineage-commitment and aberrant epigenetic repression of late differentiation genes. DNA hypomethylation in response to decitabine was greatest at CpGs that are hypomethylated during normal myeloid differentiation. In contrast, normal HSPC treated with decitabine retained immature morphology, and methylation significantly decreased at CpG that are hypermethylated during myeloid differentiation. Partial differentiation at baseline, and repression of key late differentiation genes by epigenetic means, likely plays a role in methylation and phenotype responses of AML cells treated with decitabine. Bisulphite converted DNA from the 208 samples were hybridised to the Illumina Cancel Panel 1 GPL9183 methylation assay

2011-07-01 | E-GEOD-29047 | biostudies-arrayexpress

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