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Graphdiyne oxide nanosheets display anti-leukemia efficacy specifically against DNMT3A-mutant AML cells [Bisulfite-Seq]

ABSTRACT: Acute myeloid leukemia (AML) is a fatal hematological malignancy for most patients, and DNA methyltransferase 3A (DNMT3A) mutations occur in about 30-35% of AML patients. We show graphdiyne oxide (GDYO), a member of two-dimensional carbon nanomaterials3, demonstrates an anti-leukemia effect in vitro and in vivo against AML cells with DNMT3A mutation specifically. Here, we used reduced representation bisulfite sequencing (RRBS) to depict DNA methylome of AML cells with or without GDYO treatment.

ORGANISM(S): Homo sapiens

PROVIDER: GSE190873 | GEO | 2022/08/23

REPOSITORIES: GEO

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Graphdiyne oxide nanosheets display anti-leukemia efficacy specifically against DNMT3A-mutant AML cells [RNA-Seq]

Project description:Acute myeloid leukemia (AML) is a fatal hematological malignancy for most patients, and DNA methyltransferase 3A (DNMT3A) mutations occur in about 30-35% of AML patients. We show graphdiyne oxide (GDYO), a member of two-dimensional carbon nanomaterials3, demonstrates an anti-leukemia effect in vitro and in vivo against AML cells with DNMT3A mutation specifically. Here, we used RNA-seq to depict transcriptome of AML cells with or without GDYO treatment.

2022-08-23 | GSE190871 | GEO

Graphdiyne oxide nanosheets display anti-leukemia efficacy specifically against DNMT3A-mutant AML cells

Project description:Graphdiyne oxide nanosheets display anti-leukemia efficacy specifically against DNMT3A-mutant AML cells

| PRJNA788776 | ENA

Graphdiyne oxide nanosheets display anti-leukemia efficacy specifically against DNMT3A-mutant AML cells [Bisulfite-Seq]

Project description:Graphdiyne oxide nanosheets display anti-leukemia efficacy specifically against DNMT3A-mutant AML cells [Bisulfite-Seq]

| PRJNA788779 | ENA

Graphdiyne oxide nanosheets display anti-leukemia efficacy specifically against DNMT3A-mutant AML cells [RNA-Seq]

Project description:Graphdiyne oxide nanosheets display anti-leukemia efficacy specifically against DNMT3A-mutant AML cells [RNA-Seq]

| PRJNA788781 | ENA

Graphdiyne oxide nanosheets display anti-leukemia efficacy specifically against DNMT3A-mutant AML cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-08-23 | GSE190874 | GEO

Differential genomic-methylation profile of EOL-1 cells transduced with WT/mutant-DNMT3A

Project description:DNA methyltransferase 3A (DNMT3A) gene is mutated in various myeloid neoplasms including acute myeloid leukemia (AML), especially at the Arg882 and associated with inferior outcomes. Here we wished to perform the differential genomic-methylation profile in EOL-1 cells over-expressed with DNMT3A-Arg882Cys(R882C) and DNMT3A-Ser714Cys (S714C) mutations including DNMT3A-WT and vector. Results: Differential genomic-methylation assess identified both hypo- and hypermethylation features in different regions throughout the whole genome of DNMT3A mutants-transduced EOL-1 cells.

2020-01-31 | GSE109364 | GEO

Hotspot DNMT3A and IDH1/2 Mutations in Acute Myeloid Leukemia and Their Relevance as Targets for Immunotherapy

Project description:DNA methyltransferase 3A (DNMT3A) and isocitrate dehydrogenase 1 & 2 (IDH1/2) are genes involved in epigenetic regulation, each mutated in 7-23% of acute myeloid leukemia (AML). Here, we investigated whether hotspot mutations in these genes encode neoantigens that can be targeted by immunotherapy. Five EBV-B cell lines expressing common HLA class I alleles were transduced with a minigene construct containing mutations that often occur in DNMT3A or IDH1/2. Peptides eluted from HLA class I alleles on these EBV-B cell lines were analyzed by tandem mass spec-trometry. We identified an HLA-A*01:01-binding DNMT3AR882H peptide and HLA-B*07:02-binding IDH2R140Q peptide, for which we searched for specific T cells in healthy individuals using pep-tide-HLA tetramers. Various T-cell clones were isolated showing specific reactivity against cell lines transduced with full-length DNMT3AR882H or IDH2R140Q genes, while cell lines transduced with wildtype genes were not recognized. One T-cell clone for DNMT3AR882H also reacted against patient AML cells with the mutation, while AML cells without the mutation were not recognized, thereby validating surface presentation of a DNMT3AR882H neoantigen that can potentially be targeted on HLA-A*01:01 positive AML by immunotherapy.

2024-06-23 | PXD050560 | Pride

Differential gene expression profile in U937 cells transduced with WT/mutant-DNMT3A

Project description:DNA methyltransferase 3A (DNMT3A) gene is mutated in various myeloid neoplasms including acute myeloid leukemia (AML), especially at the Arg882 and associated with inferior outcomes. Despite the current progress of functional role of DNMT3A mutations, the molecular pathogenesis of myeloid malignancies remains poorly understood. The mechanisms of AML transformation and functional role of DNMT3A mutations through its target genes in the leukemogenesis remain to be explored. Here we wished to perform the differential gene expression profile in U937 cells over-expressed with DNMT3A-Arg882His/Cys (R882H/C) mutations including DNMT3A-WT and vector. Results: Gene expression profiling analysis revealed aberrant expression of several cell-cycle and apoptosis-related genes in U937 cells transduced with mutant DNMT3A compared to WT- or vector control.

2017-12-01 | GSE90931 | GEO

Differential genomic-methylation profile of U937 cells transduced with WT/mutant-DNMT3A

Project description:DNA methyltransferase 3A (DNMT3A) gene is mutated in various myeloid neoplasms including acute myeloid leukemia (AML), especially at the Arg882 and associated with inferior outcomes. Despite the current progress of functional role of DNMT3A mutations, the molecular pathogenesis of myeloid malignancies remains poorly understood. The mechanisms of AML transformation and functional role of DNMT3A mutations through its target genes in the leukemogenesis remain to be explored. Here we wished to perform the differential genomic-methylation profile in U937 cells over-expressed with DNMT3A-Arg882His/Cys (R882H/C) mutations including DNMT3A-WT and vector using Illumina MethylationEPIC BeadChip microarray. Results: Differential genomic-methylation assess identified both hypo- and hypermethylation features in different regions throughout the whole genome of DNMT3A mutants-transduced U937 cells.

2017-12-01 | GSE90933 | GEO

STING Mediates Increased Self-Renewal and Lineage Skewing in DNMT3A-Mutated Hematopoietic Stem/Progenitor Cells

Project description:Somatic mutations in DNA methyltransferase 3A (DNMT3A) are frequently observed in patients with hematological malignancies. Hematopoietic stem/progenitor cells (HSPCs) with mutated DNMT3A demonstrate increased self-renewal activity and skewed lineage differentiation. However, the molecular mechanisms underlying these changes remain largely unexplored. In this study, we show that Dnmt3a loss leads to the upregulation of endogenous retroviruses (ERVs) in HSPCs, subsequently activating the cGAS-STING pathway and triggering inflammatory responses in these cells. Both genetic and pharmacological inhibition of STING effectively corrects the increased self-renewal activity and differentiation skewing induced by Dnmt3a deficiency in mice. Notably, targeting STING showed inhibited acute myeloid leukemia (AML) development in a Dnmt3a-KO; Flt3-ITD AML model, comparable to AC220, an FDA-approved FLT3-ITD inhibitor. A patient-derived xenograft (PDX) model further demonstrated that targeting STING effectively alleviates the leukemic burden of DNMT3A-mutant AML. Collectively, our findings highlight a critical role for STING in hematopoietic disorders induced by DNMT3A mutations and propose STING as a potential therapeutic target for preventing the progression of DNMT3A mutation-associated leukemia.

2024-12-19 | GSE278208 | GEO

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