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A stem cell model identifies two alternative cell fates in CBFA2T3::GLIS2-driven acute megakaryoblastic leukemia initiation (ChIP-seq)

ABSTRACT: A stem cell model identifies two alternative cell fates in CBFA2T3::GLIS2-driven acute megakaryoblastic leukemia initiation (ChIP-seq)

PROVIDER: PRJNA1160181 | ENA |

REPOSITORIES: ENA

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CBFA2T3::GLIS2 pediatric acute megakaryoblastic leukemia is sensitive to BCL-XL inhibition by navitoclax and DT2216

Project description:We engineered human models of CBFA2T3::GLIS2 acute megakaryoblastic leukemia and compared gene expression profiles to primary pediatric samples.

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A stem cell model identifies two alternative cell fates in CBFA2T3::GLIS2-driven acute megakaryoblastic leukemia initiation (scRNA-seq)

Project description:CBFA2T3::GLIS2 (CG) is an oncogenic fusion protein found in high-risk pediatric acute megakaryoblastic leukemia (AMKL). To gain insight into its leukemogenic mechanism, we developed a disease model based on genetically modified human induced pluripotent stem cells. We found that CG expression disrupts myeloid differentiation in this model via two alternate paths: either by delaying differentiation of aberrant megakaryocytes (aMK) or by locking aberrant megakaryocyte progenitors (aMKP) in a proliferative state akin to AMKL tumor cells. We characterized the gene-regulatory networks characterizing both cell states by single-cell and epigenome analysis, and observed that CG sustains aMKPs along with cooperators GATA2 and ERG, while repressing differentiation factors like CEBPA, LYL1, and NFE2. In contrast, aMKs maintained many differentiation factors and did not up-regulate regulators of self-renewal. In future, our findings may contribute to improved diagnostic and therapeutic procedures aimed at interconverting cell states in CG-positive patients.

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Project description:CBFA2T3::GLIS2 (CG) is an oncogenic fusion protein found in high-risk pediatric acute megakaryoblastic leukemia (AMKL). To gain insight into its leukemogenic mechanism, we developed a disease model based on genetically modified human induced pluripotent stem cells. We found that in this model CG expression disrupts myeloid differentiation via two alternate paths: either by delaying differentiation of aberrant megakaryocytes (aMK) or by locking aberrant megakaryocyte progenitors (aMKP) in a proliferative state akin to AMKL tumor cells. We defined the gene-regulatory networks characterizing both cell states by single-cell transcriptome and epigenome analysis and observed that CG sustains aMKP self-renewal along with cooperators like GATA2 and ERG, while repressing differentiation factors such as SPI1, CEBPA, NFE2, and LYL1. In contrast, in aMKs, CG downregulated drivers of self-renewal and upregulated most but not all lineage-specific differentiation factors. Our findings may contribute to strategies selectively targeting the aMKP state in CG-AMKL patients.

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A stem cell model identifies two alternative cell fates in CBFA2T3::GLIS2-driven acute megakaryoblastic leukemia initiation (ChIP-seq)

Project description:CBFA2T3::GLIS2 (CG) is an oncogenic fusion protein found in high-risk pediatric acute megakaryoblastic leukemia (AMKL). To gain insight into its leukemogenic mechanism, we developed a disease model based on genetically modified human induced pluripotent stem cells. We found that in this model CG expression disrupts myeloid differentiation via two alternate paths: either by delaying differentiation of aberrant megakaryocytes (aMK) or by locking aberrant megakaryocyte progenitors (aMKP) in a proliferative state akin to AMKL tumor cells. We defined the gene-regulatory networks characterizing both cell states by single-cell transcriptome and epigenome analysis and observed that CG sustains aMKP self-renewal along with cooperators like GATA2 and ERG, while repressing differentiation factors such as SPI1, CEBPA, NFE2, and LYL1. In contrast, in aMKs, CG downregulated drivers of self-renewal and upregulated most but not all lineage-specific differentiation factors. Our findings may contribute to strategies selectively targeting the aMKP state in CG-AMKL patients.

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A stem cell model identifies two alternative cell fates in CBFA2T3::GLIS2-driven acute megakaryoblastic leukemia initiation (RNA-seq)

Project description:CBFA2T3::GLIS2 (CG) is an oncogenic fusion protein found in high-risk pediatric acute megakaryoblastic leukemia (AMKL). To gain insight into its leukemogenic mechanism, we developed a disease model based on genetically modified human induced pluripotent stem cells. We found that in this model CG expression disrupts myeloid differentiation via two alternate paths: either by delaying differentiation of aberrant megakaryocytes (aMK) or by locking aberrant megakaryocyte progenitors (aMKP) in a proliferative state akin to AMKL tumor cells. We defined the gene-regulatory networks characterizing both cell states by single-cell transcriptome and epigenome analysis and observed that CG sustains aMKP self-renewal along with cooperators like GATA2 and ERG, while repressing differentiation factors such as SPI1, CEBPA, NFE2, and LYL1. In contrast, in aMKs, CG downregulated drivers of self-renewal and upregulated most but not all lineage-specific differentiation factors. Our findings may contribute to strategies selectively targeting the aMKP state in CG-AMKL patients.

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A stem cell model identifies two alternative cell fates in CBFA2T3::GLIS2-driven acute megakaryoblastic leukemia initiation

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2012-11-20 | E-GEOD-35203 | biostudies-arrayexpress

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