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Loss of DKM6A confers drug resistance in acute myeloid leukemia (ChIP-seq of AML cell lines MM-1 and MM-6)

ABSTRACT: Loss of DKM6A confers drug resistance in acute myeloid leukemia (ChIP-seq of AML cell lines MM-1 and MM-6)

PROVIDER: PRJNA526903 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8723510.fastq.gz	Fastqsanger.gz
	SRR8723511.fastq.gz	Fastqsanger.gz
	SRR8723512.fastq.gz	Fastqsanger.gz
	SRR8723513.fastq.gz	Fastqsanger.gz
	SRR8723514.fastq.gz	Fastqsanger.gz

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Loss of DKM6A confers drug resistance in acute myeloid leukemia (ChIP-seq of AML cell lines MM-1 and MM-6)

Project description:Acute myeloid leukemia (AML) is an aggressive hematologic neoplasm resulting from the malignant transformation of myeloid progenitors. Despite intensive chemotherapy leading to initial treatment responses, relapse caused by intrinsic or acquired drug resistance represents a major challenge. Here, we report that histone 3 lysine 27 demethylase KDM6A (UTX) is targeted by inactivating mutations and mutation-independent regulation in relapsed AML. Analyses of matched diagnosis and relapse specimens from individuals with KDM6A mutations showed an outgrowth of the KDM6A mutated tumor population at relapse. KDM6A-null myeloid leukemia cells were more resistant to treatment with the chemotherapeutic agents cytarabine (AraC) and daunorubicin. Inducible re-expression of KDM6A in KDM6A-null cell lines suppressed proliferation and sensitized cells again to AraC treatment. RNA expression analysis and functional studies revealed that resistance to AraC was conferred by downregulation of the nucleoside membrane transporter ENT1 (SLC29A1). Our results show that loss of KDM6A provides cells with a selective advantage during chemotherapy, which ultimately leads to the observed outgrowth of clones with KDM6A mutations or reduced KDM6A expression at relapse.

2019-06-18 | GSE128259 | GEO

Loss of DKM6A confers drug resistance in acute myeloid leukemia

Project description:Loss of DKM6A confers drug resistance in acute myeloid leukemia

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Loss of DKM6A confers drug resistance in acute myeloid leukemia (ChIP-seq of AML cell lines K562 and THP-1)

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Loss of DKM6A confers drug resistance in acute myeloid leukemia (ChIP-seq of AML cell lines K562 and THP-1)

Project description:Loss of DKM6A confers drug resistance in acute myeloid leukemia (ChIP-seq of AML cell lines K562 and THP-1)

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Gata2 promotes drug resistance in Acute Myeloid Leukemia (AML)

Project description:In this study, we generated mouse models of MLL-AF9-driven AML (MA9) harboring conditional alleles for Gata2 gene to precisely investigate the role of Gata2 in drug resistance and progression of MLL-rearranged (MLL-r) AML. Our findings revealed a novel mechanism for Gata2 in blunting p53 mediated apoptosis via transcriptional repression of Rassf4, a regulator of Mdm2 protein stability.

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Gata2 promotes drug resistance in Acute Myeloid Leukemia (AML)

Project description:Gata2 promotes drug resistance in Acute Myeloid Leukemia (AML)

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Gata2 promotes drug resistance in Acute Myeloid Leukemia (AML) [ChIP-Seq]

Project description:Gata2 promotes drug resistance in Acute Myeloid Leukemia (AML) [ChIP-Seq]

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mRNA-sequencing in drug-resistant acute myeloid leukemia

Project description:mRNA sequencing for AML cells(HL-60) and drug-resistant AML Cells(HL60/MX2).

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Efficacy of novel agents against cellular models of familial platelet disorder with myeloid malignancy (FPD-MM). [ChIP-Seq]

Project description:Germline, mono-allelic mutations in RUNX1 cause familial platelet disorder (RUNX1-FPD) that evolves into myeloid malignancy (FPD-MM): MDS or AML. FPD-MM commonly harbors co-mutations in the second RUNX1 allele and/or other epigenetic regulators. Here we utilized patient-derived (PD) FPD-MM cells and established the first FPD-MM AML cell line (GMR-AML1). GMR-AML1 cells exhibited active super-enhancers of MYB, MYC, BCL2 and CDK6, augmented expressions of c-Myc, c-Myb, EVI1 and PLK1 and surface markers of AML stem cells. In longitudinally studied bone marrow cells from a patient at FPD-MM vs RUNX1-FPD state, we confirmed increased chromatin accessibility and mRNA expressions of MYB, MECOM and BCL2 in FPD-MM cells. GMR-AML1 and PD FPD-MM cells were sensitive to homoharringtonine (HHT or omacetaxine) or mebendazole-induced lethality, associated with repression of c-Myc, EVI1, PLK1, CDK6 and MCL1. Co-treatment with MB and the PLK1 inhibitor volasertib exerted synergistic in vitro lethality in GMR-AML1 cells. In luciferase-expressing GMR-AML1 xenograft model, MB, omacetaxine or volasertib monotherapy, or co-treatment with MB and volasertib, significantly reduced AML burden and improved survival in the immune-depleted mice. These findings highlight the molecular features of FPD-MM progression and demonstrate HHT, MB and/or volasertib as effective agents against cellular models of FPD-MM.

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