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Epigenome of ASXL1-mutant and ASXL1-wildtype chronic myelomonocytic leukemia

ABSTRACT: Epigenome of ASXL1-mutant and ASXL1-wildtype chronic myelomonocytic leukemia

PROVIDER: PRJNA670720 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17155500_1.fastq.gz	Fastqsanger.gz
	SRR17155500_2.fastq.gz	Fastqsanger.gz
	SRR17155600_1.fastq.gz	Fastqsanger.gz
	SRR17155600_2.fastq.gz	Fastqsanger.gz
	SRR17155501_1.fastq.gz	Fastqsanger.gz

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Transcriptome of ASXL1-mutant and ASXL1-wildtype chronic myelomonocytic leukemia

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Epigenome of ASXL1-mutant and ASXL1-wildtype chronic myelomonocytic leukemia

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Prognostic interaction between ASXL1 and TET2 mutations in chronic myelomonocytic leukemia.

Project description:Mutations involving epigenetic regulators (TET2~60% and ASXL1~40%) and splicing components (SRSF2~50%) are frequent in chronic myelomonocytic leukemia (CMML). On a 27-gene targeted capture panel performed on 175 CMML patients (66% males, median age 70 years), common mutations included: TET2 46%, ASXL1 47%, SRSF2 45% and SETBP1 19%. A total of 172 (98%) patients had at least one mutation, 21 (12%) had 2, 24 (14%) had 3 and 30 (17%) had >3 mutations. In a univariate analysis, the presence of ASXL1 mutations (P=0.02) and the absence of TET2 mutations (P=0.03), adversely impacted survival; while the number of concurrent mutations had no impact (P=0.3). In a multivariable analysis that included hemoglobin, platelet count, absolute monocyte count and circulating immature myeloid cells (Mayo model), the presence of ASXL1 mutations (P=0.01) and absence of TET2 mutations (P=0.003) retained prognostic significance. Patients were stratified into four categories: ASXL1wt/TET2wt (n=56), ASXL1mut/TET2wt (n=31), ASXL1mut/TET2mut (n=50) and ASXL1wt/TET2mut (n=38). Survival data demonstrated a significant difference in favor of ASXL1wt/TET2mut (38 months; P=0.016), compared with those with ASXL1wt/TET2wt (19 months), ASXL1mut/TET2wt (21 months) and ASXL1mut/TET2mut (16 months) (P=0.3). We confirm the negative prognostic impact imparted by ASXL1 mutations and suggest a favorable impact from TET2 mutations in the absence of ASXL1 mutations.

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Expression of mutant Asxl1 perturbs hematopoiesis and promotes susceptibility to leukemic transformation

Project description:Additional Sex Combs Like 1 (ASXL1) is frequently mutated in myeloid malignancies and clonal hematopoiesis of indeterminate potential (CHIP). Although loss of ASXL1 promotes hematopoietic transformation, there is growing evidence that ASXL1 mutations might confer an alteration of function. Here we identify that physiological expression of a C-terminal truncated Asxl1 mutant in vivo using conditional knock-in (KI) results in myeloid skewing, age-dependent anemia, thrombocytosis, and morphologic dysplasia. Although expression of mutant Asxl1 altered the functions of hematopoietic stem cells (HSCs), it maintained their survival in competitive transplantation assays and increased susceptibility to leukemic transformation by co-occurring RUNX1 mutation or viral insertional mutagenesis. KI mice displayed substantial reductions in H3K4me3 and H2AK119Ub without significant reductions in H3K27me3, distinct from the effects of Asxl1 loss. ChIP-seq analysis demonstrated opposing effects of wildtype and mutant Asxl1 on H3K4me3. These findings reveal that ASXL1 mutations confer HSCs with an altered epigenome and increase susceptibility for leukemic transformation, presenting a novel model for CHIP.

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Project description:BackgroundMolecular genetic abnormalities are observed in over 90% of chronic myelomonocytic leukemia (CMML) cases. Recently, several studies have demonstrated the negative prognostic impact of ASXL1 mutations in CMML patients. We evaluated the prognostic impact of ASXL1 mutations and compared five CMML prognostic models in Korean patients with CMML.MethodsWe analyzed data from 36 of 57 patients diagnosed as having CMML from January 2000 to March 2016. ASXL1 mutation analysis was performed by direct sequencing, and the clinical and laboratory features of patients were compared according to ASXL1 mutation status.ResultsASXL1 mutations were detected in 18 patients (50%). There were no significant differences between the clinical and laboratory characteristics of ASXL1-mutated (ASXL1?) CMML and ASXL1-nonmutated (ASXL1?) CMML patients (all P>0.05). During the median follow-up of 14 months (range, 0-111 months), the overall survival (OS) of ASXL1? CMML patients was significantly inferior to that of ASXL1? CMML patients with a median survival of 11 months and 19 months, respectively (log-rank P=0.049). An evaluation of OS according to the prognostic models demonstrated inferior survival in patients with a higher risk category according to the Mayo molecular model (log-rank P=0.001); the other scoring systems did not demonstrate a significant association with survival.ConclusionsWe demonstrated that ASXL1 mutations, occurring in half of the Korean CMML patients examined, were associated with inferior survival. ASXL1 mutation status needs to be determined for risk stratification in CMML.

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Functional study on the cooperation of ASXL1 and RUNX1 mutations for myeloid leukemia transformation

Project description:BACKGROUND: Our previous studies showed that RUNX1 and ASXL1 mutations were frequently co-existed in chronic myelomonocytic leukemia (CMML) and clonal evolution of RUNX1 and/or ASXL1 occurred most frequently in chronic myeloid leukemia (CML) with myeloid blastic crisis. The molecular pathogenesis of cooperation of RUNX1 and ASXL1 mutations has not been reported yet. METHODS: Lentiviral-mediated stable transduction of RUNX1-WT/MT (R135T) in K562 cells which harboring ASXL1-MT (Y591X). RNA was extracted from stable cell line and used for gene-expression microarray analysis. RESULTS: For in vitro study, we overexpressed RUNX1-WT/MT (R135T) in K562 cells which harboring ASXL1-MT (Y591X). We found that RUNX1-MT augmented cell proliferation, colony formation, HOXA gene expression and inhibited megakaryocytic differentiation in ASXL1-MT K562 cells compared to RUNX1-WT or empty vector control. We performed gene expression profile of K562 cells overexpressed with EV, RUNX1-WT and RUNX1-R135T mutation. Gene expression microarray data revealed that 147 genes upregulated more than 2-fold in RUNX1-R135T expressing K562 cells compared to EV control cells. From gene expression data analysis, we found that inhibitor of DNA binding 1 (ID1), a key transcriptional regulator of hematopoietic stem cell (HSC) lineage commitment, is upregulated in RUNX1-R135T-transduced K562 cells compared to EV and RUNX1-WT-expressing cells.

2018-06-01 | GSE99640 | GEO

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