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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE187291 | GEO | 2022/11/30

REPOSITORIES: GEO

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

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

Gene expression profiling upon treatment with NTX-301

2022-04-20 | GSE188392 | GEO

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 in MV4-11

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

| PRJNA777427 | ENA

The Effect of Decitabine and ATRA on the Methylome in the AML cell line U-937

Project description:The combination of the demethylating agent Decitabine (DAC) and the retinoic acid ATRA has shown potent antileukemic action both in vitro and in vivo. The likely synergistic mechanism of action remains unknown. Both DAC and retinoid acids are known to affect methylation. DAC inhibits DNA-methyltransferases by covalent bonding, thereby causing demethylation after several replication cycles (Stresemann and Lyko, 2008). Depending on gene and entity, both demethylation (Das et al., 2010; Di Croce et al., 2002) as well as hypermethylation (Das et al., 2010) have been induced by treatment with retinoids. Therefore, a synergistic mechanism of action regarding the methylome to explain the combinatorial strong antileukemic effect of DAC+ATRA was investigated.

2022-06-30 | GSE181960 | GEO

LC-MSMS of the MHC-I immunopeptidome of AML cell line, THP-1

Project description:The hypomethylating agent 5-azacytidine (AZA) is the first-line induction therapy for AML patients unsuitable for intensive chemotherapy. The anti-tumor effect of AZA results in part from T-cell cytotoxic responses against MHC-I-associated peptides (MAPs) deriving from hypermethylated genomic regions such as cancer-testis antigens (CTAs), or endogenous retroelements (EREs). However, clear evidence supporting higher ERE MAPs presentation after AZA treatment in AML is lacking. Interestingly, we find that AZA-mediated DNMT2 inhibition leads to autophagy induction, which is responsible for mitigating ERE MAPs generation. To validate our findings, we examined the immunopeptidome of THP-1 cells treated with AZA combined with autophagy inhibitor, Spautin-1 or decitabine (DAC, non-DNMT2 inhibiting HMA) through a proteogenomic approach.

2024-04-17 | PXD046853 | Pride

Transcriptional profile of AML xenografts treated with either PBS or a combination of decitabine and cytarabine

Project description:The Affymetrix Human Genome U133 Plus 2.0 Array was used to examine the Genome wide transcriptional changes which follow the treatment of AML xenografts with either PBS control or combination of decitabine (DAC) and cytarabine (Ara-C). Animals were treated with PBS, DAC alone, Ara-C alone, DAC and Ara-C combined (D+A), DAC followed by Ara-C (D/A) or Ara-C followed by DAC (A/D). PBS vs each drug combination

2013-03-06 | E-GEOD-44857 | 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

Transcriptional profile of AML xenografts treated with either PBS or a combination of decitabine and cytarabine

2013-03-06 | GSE44857 | GEO

RNA-seq in KPC mice treated with a hypomethylating drug (decitabine) and in untreated KPC mice

Project description:Background: Treatment with single-agent decitabine (5aza-dC; DAC), a well-tolerated DNA hypomethylating drug, in a mouse model of pancreatic ductal adenocarcinoma (PDAC), KPC-Brca1, extended the survival of the animals and upregulated immune-related pathways. Here we extend these findings to combination therapy, using DAC followed by the immune checkpoint inhibitor anti-PD-1H in the original more widely utilized KPC (Pdx-Cre Kras/p53) model. Methods: We treated tumor-bearing KPC mice with DAC, and with anti-PD-1H, separately and in combination, and assessed tumor growth, mouse survival, immune cell infiltration of the tumors, and gene expression, compared to historical and mock-treated control mice. Results: Treatment with single-agent DAC led to increased Cd8+ tumor-infiltrating T cells (TILs), increased tumor necrosis, and slower tumor growth. RNA-seq analysis revealed increased expression of a group of myeloid-lineage markers, including Chi3l3 (Ym1), which proved to reflect recruitment or expansion of a unique population of Chi3l3/Arginase-1 double-positive “M2-polarized” tumor-infiltrating myeloid cells. Anti-PD-1H alone had only modest effects on tumor growth and number of Cd8+ TILs. However, PD-1H-expressing TILs were significantly increased by single agent DAC, and DAC treatment followed by anti-PD-1H produced the strongest increase in Cd8+ TILS, inhibition of tumor growth, and prolongation of survival. Conclusions: Treatment with DAC alone, and DAC plus anti-PD-1H, inhibits PDAC tumor growth in the KPC model and produces changes in tumor-infiltrating lymphoid and myeloid cell populations, with an additive therapeutic benefit from combining the two agents. Since the influx of M2-polarized macrophages induced by DAC is predicted to antagonize the anti-tumor effects, future work should investigate eliminating or reprogramming these cells.

2018-07-01 | GSE101336 | GEO

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