DNA methylation profiling upon treatment with NTX-301 or decitabine in AML cells
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PROVIDER: PRJNA777433 | ENA |
REPOSITORIES: ENA
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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
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
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 MV4-11 cell line.
2022-04-20 | GSE187285 | GEO
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
Project description:DNA hypomethylating agents (HMAs) are used to treat acute myeloid leukaemia (AML) and myelodysplasia patients who are unsuitable for intensive chemotherapy, but low response rates and therapy-resistant relapse remain significant challenges. To optimise HMA efficacy, we must understand how resistance and relapse arise from cells that survive treatment. Here we combine single-cell multi-omic analysis with parallel colony-forming assays to link HMA-induced molecular heterogeneity with functional consequences in AML cells. HMAs, azacytidine (azacytidine) and decitabine (decitabine), induced global epigenetic heterogeneity associated with upregulation of inflammatory responses and cell death pathways in a subset of hypomethylated cells. Some AML cells maintained high DNA methylation during treatment, and these methylation-retaining cells had increased self-renewal capacity following decitabine, but not azacytidine. Molecular profiling of individual colonies revealed upregulated cholesterol biosynthesis as an adaptation to HMA treatment, and inhibition by rosuvastatin enhanced decitabine effects in vitro and in vivo. Thus, HMA-induced heterogeneity has important implications for AML cell growth and statins are a candidate co-treatment strategy to delay or prevent HMA-resistant relapse.
2025-07-22 | GSE260868 | GEO
Project description:DNA hypomethylating agents (HMAs) are used to treat acute myeloid leukaemia (AML) and myelodysplasia patients who are unsuitable for intensive chemotherapy, but low response rates and therapy-resistant relapse remain significant challenges. To optimise HMA efficacy, we must understand how resistance and relapse arise from cells that survive treatment. Here we combine single-cell multi-omic analysis with parallel colony-forming assays to link HMA-induced molecular heterogeneity with functional consequences in AML cells. HMAs, azacytidine cytidine (azacytidine ) and decitabine (decitabine ), induced global epigenetic heterogeneity associated with upregulation of inflammatory responses and cell death pathways in a subset of hypomethylated cells. Some AML cells maintained high DNA methylation during treatment, and these methylation-retaining cells had increased self-renewal capacity following decitabine , but not azacytidine . Molecular profiling of individual colonies revealed upregulated cholesterol biosynthesis as an adaptation to HMA treatment, and inhibition by rosuvastatin enhanced decitabine effects in vitro and in vivo. Thus, HMA-induced heterogeneity has important implications for AML cell growth and statins are a candidate co-treatment strategy to delay or prevent HMA-resistant relapse.
2025-07-22 | GSE256353 | GEO
Project description:DNA hypomethylating agents (HMAs) are used to treat acute myeloid leukaemia (AML) and myelodysplasia patients who are unsuitable for intensive chemotherapy, but low response rates and therapy-resistant relapse remain significant challenges. To optimise HMA efficacy, we must understand how resistance and relapse arise from cells that survive treatment. Here we combine single-cell multi-omic analysis with parallel colony-forming assays to link HMA-induced molecular heterogeneity with functional consequences in AML cells. HMAs, azacytidine cytidine (azacytidine ) and decitabine (decitabine ), induced global epigenetic heterogeneity associated with upregulation of inflammatory responses and cell death pathways in a subset of hypomethylated cells. Some AML cells maintained high DNA methylation during treatment, and these methylation-retaining cells had increased self-renewal capacity following decitabine , but not azacytidine . Molecular profiling of individual colonies revealed upregulated cholesterol biosynthesis as an adaptation to HMA treatment, and inhibition by rosuvastatin enhanced decitabine effects in vitro and in vivo. Thus, HMA-induced heterogeneity has important implications for AML cell growth and statins are a candidate co-treatment strategy to delay or prevent HMA-resistant relapse.
2025-07-22 | GSE263049 | GEO
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
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
Project description:Gene expression profiling upon treatment with NTX-301
| PRJNA778722 | ENA