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Gene expression of bone marrow cells from PHF6-deficiency of RUNX1-ETO9a induced acute myeloid leukemia mouse model

ABSTRACT: Gene expression of bone marrow cells from PHF6-deficiency of RUNX1-ETO9a induced acute myeloid leukemia mouse model

PROVIDER: PRJNA843971 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19450187_1.fastq.gz	Fastqsanger.gz
	SRR19450187_2.fastq.gz	Fastqsanger.gz
	SRR19450188_1.fastq.gz	Fastqsanger.gz
	SRR19450188_2.fastq.gz	Fastqsanger.gz
	SRR19450189_1.fastq.gz	Fastqsanger.gz

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Gene expression of bone marrow cells from PHF6-deficiency of RUNX1-ETO9a induced acute myeloid leukemia mouse model

Project description:To explore the underlying molecular mechanisms of Phf6 loss in delaying AML progression, we analyzed the transcriptional profiles of VC Phf6,RE9a and WT Phf6,RE9a AML cells via RNA-sequencing

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Synergism 1 between RUNX1 and PHF6 mutations in leukemogenesis [scRNAseq]

Project description:RUNX family transcription factor 1 (RUNX1) mutated acute myeloid leukemia (AML) has now been formally classified as AML with myelodysplasia-related gene mutations, and considered to predict adverse prognosis. In addition, mutations of RUNX1 and plant homeodomain finger gene 6 (PHF6) frequently co-occurred and conferred particularly adverse clinical outcomes. Becasue the pathological effects of these combined mutations remained understudied, we sought to address this topic through genetically modified mouse models. We found that Phf6 knockout and RUNX1 double-mutated bone marrow (BM) cells displayed significantly higher engraftment capacity, and recipient mice transplanted with double-mutated BM cells developed AML with significantly shortened survival. We also discovered that the multipotent progenitors (MPPs) were the main cell subpopulation responsible for double-mutated BM cell-induced leukemia. Our findings highlighted the synergistic leukemogenic potential of Phf6 and RUNX1 mutations in vivo, and provided evidence for possible underlying molecular mechanisms.

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Molecular and clinical analyses of PHF6 mutant myeloid neoplasia provide clues as to their pathogenesis and therapeutic targeting

Project description:PHF6 mutations (PHF6MT) are identified in various myeloid neoplasms (MN). However, little is known about the precise function and consequences of PHF6 in MN. Our comprehensive genomic analyses focused on three main findings. Firstly, we revealed a different pattern of genes correlating with PHF6MT in male and female cases. When analyzing male and female cases separately, in only male cases, RUNX1 and U2AF1 were co-mutated with PHF6. In contrast, female cases revealed co-occurrence of ASXL1 mutations and X-chromosome deletions with PHF6MT. Next, proteomics analysis revealed a direct interaction between PHF6 and the pioneer transcription factor RUNX1. Both proteins co-localize in active enhancer regions that define the context of lineage differentiation. Finally, we demonstrated a negative prognostic role of PHF6MT, especially in association with RUNX1. The negative effects on survival were additive as PHF6MT cases with RUNX1 mutations had worse outcomes when compared to cases carrying single mutation or wild-type.

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Synergism 1 between RUNX1 and PHF6 mutations in leukemogenesis [scRNAseq]

Project description:Synergism 1 between RUNX1 and PHF6 mutations in leukemogenesis [scRNAseq]

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Single-cell RNA sequencing of RUNX1-RUNX1T1(9a) transformed mouse bone marrow cells

Project description:Single-cell RNA sequencing analysis of RUNX1-RUNX1T1(9a) transformed c-kit positive cells with (Kat2a WT) and without Kat2a (Kat2a NULL). Lineage negative bone marrow cells were collected from Kat2a fl/fl Mx1-Cre-/- and Kat2a fl/fl Mx1-Cre +/- animals after pIpC treatment and transduced with RUNX1-RUNX1T1(9a) expressing retrovirus (reported by GFP expression). Cells were injected into irradiated C57BL6 mice and GFP positive c-Kit positive bone marrow cells collected 2 and 4 months after transplantation. Cells were processed for single-cell RNA sequencing library preparation (10X chromium single cell) and next gene sequencing following 10X genomics v2 protocol.

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Project description:The study profiled the effect of Phf6 deletion on gene expression in hematopoietic stem cells (HSCs), multipotent progenitor cells (MPPs) and hematopoietic progenitor cells (HPC-1). Phf6lox/Y;Tie2-creTg/+ mice were prepared on a C57BL/6 background so that Phf6 deletion could be selectively mediated by Tie2-cre. Cell populations were sorted from bone marrow samples using standard surface markers (Lin–SCA1+cKIT+(LSK) CD150+ CD48– for HSCs, Lin–SCA1+cKIT+(LSK) CD150– CD48– for MPPs and Lin–SCA1+cKIT+(LSK) CD150- CD48+ for HPC-1 cells). Phf6 intact and Phf6-delected cells of all three types were profiled by paired-end RNA-seq using an Illumina NextSeq 500 sequencer. RNA-seq libraries were prepared from the HPC-1 samples used a standard Illumina TruSeq library protocol whereas the libraries for the HSC and MPP samples used a SMART-seq ultra low input kit for cDNA synthesis and amplification. Statistical analysis of the TruSeq and SMART-seq samples was undertaken separately.

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