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Leukemic hematopoiesis

ABSTRACT: Leukemic hematopoiesis

PROVIDER: PRJNA881262 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21603800_1.fastq.gz	Fastqsanger.gz
	SRR21603800_2.fastq.gz	Fastqsanger.gz
	SRR21603900_1.fastq.gz	Fastqsanger.gz
	SRR21603900_2.fastq.gz	Fastqsanger.gz
	SRR21603801_1.fastq.gz	Fastqsanger.gz

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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:Comparative binding patterns of Chromatin Regulators in normal versus leukemic hematopoiesis [ATAC-Seq]

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Acquired TET2 mutation-linked clonal hematopoiesis in FPD/AML patient led to the development of pre-leukemic clone resulting independently in T2-ALL and AML-M0.

Project description:Germline RUNX1 mutations are found in familial platelet disorders with predisposition to acute myelogenous leukemia (FPD/AML). This very rare disease is characterized by thrombocytopenia, platelet dysfunction and a 35% lifetime risk of developing MDS/AML and in rare cases also T-ALL. Here, we focus on a case of a man with a familial history of RUNX1 R174Q mutation who developed at the age of 42 years an EGIL T2-ALL and two years after remission an AML-M0. To investigate whether initial and relapsed leukemic blasts originated from the same clone, we performed CGH array and WES on both blasts populations. In both T2-ALL and AML-M0 samples, CGH array revealed loss of 1p36.32-23 and 17q11.2 and nine other small deletions. Both AML-M0 and T2-ALL demonstrated clonal rearrangements of both TCR (V9-J1-1) and TCR (D2-J1 and D2-J3). 18 genes were found by WES to be mutated in the original clone at a frequency of more than 40%. Additional variants were identified only in T2-ALL or in AML-M0 evoking the existence of a common original clone. MiSeq technology performed on peripheral blood-derived CD34+ cells five years prior T2-ALL development revealed only missense TET2 P1962T mutation at a frequency of 1% suggesting that this mutation in association with germline RUNX1 R174Q mutation led to amplification of a hematopoietic clone susceptible to acquire other transforming alterations. Identification of clonal hematopoiesis with acquired mutations at low frequency in hematopoietic progenitors before leukemia development could clearly serve as a marker of pre-leukemic state and might be helpful in patient care.

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Project description:Aberrant Oligoclonal Hematopoiesis in Remission AML and Relapse from Rare Cells Genomically Resembling Leukemic Blasts

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Acquired TET2 mutation-linked clonal hematopoiesis in FPD/AML patient led to the development of pre-leukemic clone resulting independently in T2-ALL and AML-M0

Project description:Germline RUNX1 mutations are found in familial platelet disorders with predisposition to acute myelogenous leukemia (FPD/AML). This very rare disease is characterized by thrombocytopenia, platelet dysfunction and a 35% lifetime risk of developing MDS/AML and in rare cases also T-ALL. Here, we focus on a case of a man with a familial history of RUNX1 R174Q mutation who developed at the age of 42 years an EGIL T2-ALL and, two years after remission, an AML-M0. To investigate whether initial and relapsed leukemic blasts originated from the same clone, we performed CGH array and WES on both blasts populations. In both T2-ALL and AML-M0 samples, CGH array revealed loss of 1p36.32-23 and 17q11.2 and nine other small deletions. Both AML-M0 and T2-ALL blasts demonstrated clonal rearrangements of both TCRÎ³ (VÎ³9-JÎ³1-1) and TCRÎ´ (DÎ´2-JÎ´1 and DÎ´2-JÎ´3). 18 genes were found by WES to be mutated in both blasts at a frequency of more than 40%. Additional variants were identified only in T2-ALL or in AML-M0 evoking the existence of a common original clone, which gave rise to subclonal populations. MiSeq technology performed on peripheral blood-derived CD34+ cells five years prior T2-ALL development revealed only missense TET2 P1962T mutation at a frequency of 1% (which reaches a frequency of 50 % in fully transformed leukemic clone) suggesting that this mutation in association with germline RUNX1 R174Q mutation led to amplification of a hematopoietic clone susceptible to acquire other transforming alterations. Identification of clonal hematopoiesis with acquired mutations at low frequency in hematopoietic progenitors before leukemia development could clearly serve as a marker of pre-leukemic state and be helpful in patient care.

2017-06-29 | E-MTAB-4623 | biostudies-arrayexpress

Leukemic hematopoiesis

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

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Chromatin remodeling mediated by ARID1A is indispensable for normal hematopoiesis in mice (ChIP-Seq)

Project description:ARID1A is a component of the mammalian SWI/SNF complex involved in chromatin remodeling. A functional SWI/SNF complex is required for diverse physiological processes including hematopoiesis, however, the precise role played by ARID1A in hematopoietic development is unclear. Here we utilize hematopoietic cell-specific deletion of Arid1a in mice to uncover its role during adult hematopoiesis. We demonstrate that ARID1A is essential for maintaining the frequency and function of hematopoietic stem cells and its loss impaired the differentiation of both myeloid and lymphoid lineages. ARID1A deficiency led to a global reduction in open chromatin and ensuing transcriptional changes affected key genes involved in hematopoietic development. We also observed that silencing of ARID1A affected ATRA-induced differentiation of NB4 cells, suggesting its role in granulocytic differentiation of human leukemic cells. Overall, our study provides a comprehensive elucidation of its function in hematopoiesis and establishes ARID1A as a major regulator of chromatin dynamics in hematopoietic cells.

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