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ChIP-seq of H3K27Ac in SKNO1 cells after knockdown of ASXL2

ABSTRACT: The goals of this study are to identify the changes of H3K27Ac in SKNO1 cells after knockdown of ASXL2

ORGANISM(S): Homo sapiens

PROVIDER: GSE93164 | GEO | 2017/06/26

SECONDARY ACCESSION(S): PRJNA360173

REPOSITORIES: GEO

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ChIP-seq of H3K27me3 in SKNO1 cells after knockdown of ASXL2

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Project description:ChIP-seq of H3K27Ac in SKNO1 cells after knockdown of ASXL2

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RNA-seq of ASXL2 shRNA KD in SKNO-1 cells

Project description:The goals of this study are to compare transcriptome profiling (RNA-seq) of Asxl2 knockdowned SKNO-1 cells to control SKNO-1 cells. We found substantial number of genes are differentially expressed in Asxl2 knockdowned cells.

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ASXL2 is recurrently mutated in t(8;21) AML and regulates hematopoietic development [RNA_Seq_Asxl2_mutant]

Project description:Chromosomal translocation t(8;21) (q22;q22) leading to generation of oncogenic RUNX1-RUNX1T1 (AML1-ETO) fusion is a cytogenetic abnormality observed in about 10% of acute myelogenous leukemia (AML). To uncover somatic mutations that cooperate with t(8;21)-driven leukemia, we performed targeted and whole exome sequencing of newly-diagnosed and relapsed AML samples. We identified high frequency of truncating alterations in ASXL2 along with recurrent mutations of KIT, TET2, MGA, FLT3, and DHX15 in this subtype of AML. To investigate in-depth the role of ASXL2 in normal and malignant hematopoiesis, we utilized a mouse model of ASXL2 deficiency. Loss of ASXL2 caused progressive hematopoietic defects characterized by myeloid cell expansion, splenomegaly, extramedullary hematopoiesis and poor reconstitution ability in transplantation models. A parallel analysis of young and >1-year old Asxl2-deficient mice revealed age-dependent changes in the hematopoietic compartment leading to perturbations affecting not only myeloid and erythroid differentiation but also maturation of lymphoid cells. Our studies also suggest that expression of truncated ASXL2 protein confers proliferative advantage to mouse myeloid progenitors. Overall, these findings establish a critical role of ASXL2 in maintaining steady state hematopoiesis and provide insights into how its loss/mutation primes leukemic growth of myeloid cells.

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