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Analysis of chromatin accessibility in uncultured fetal liver hematopoietic stem-progenitor cells and upon MLLT3 overexpression [ATACseq]

ABSTRACT: MLLT3 binds to open gene TSS

ORGANISM(S): Homo sapiens

PROVIDER: GSE111480 | GEO | 2019/03/06

REPOSITORIES: GEO

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Analysis of MLLT3 genomic distribution and related chromatin features in uncultured fetal liver hematopoietic stem-progenitor cells [ChIPseq_MLLT3_OE]

Project description:MLLT3 binds to TSS of genes active in FL-HSPC

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Analysis of MLLT3 genomic distribution and related chromatin features in uncultured fetal liver hematopoietic stem-progenitor cells [ChIPseq_FL_HSPC]

Project description:MLLT3 binds to TSS of genes active in FL-HSPC

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Analysis of MLLT3 genomic distribution and related chromatin features in fetal liver hematopoietic stem-progenitor cells [ChIP-seq_cultured_FL-HSPC]

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Analysis of chromatin accessibility in uncultured fetal liver hematopoietic stem-progenitor cells and upon MLLT3 overexpression [ATACseq]

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Analysis of MLLT3 genomic distribution and related chromatin features in cultured cord blood hematopoietic stem-progenitor cells [ChIP-seq]

Project description:MLLT3 binds to TSS of genes active in CB-HSPC.

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RNA-seq of MLLT3-L and MLLT3-S overexpressing cultured HSPC, compared to non-overexpressing and uncultured FL-HSPC

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Analysis of MLLT3 genomic distribution and related chromatin features in uncultured fetal liver hematopoietic stem-progenitor cells [ChIPseq_MLLT3_OE]

Project description:Analysis of MLLT3 genomic distribution and related chromatin features in uncultured fetal liver hematopoietic stem-progenitor cells [ChIPseq_MLLT3_OE]

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Analysis of MLLT3 genomic distribution and related chromatin features in uncultured fetal liver hematopoietic stem-progenitor cells [ChIPseq_FL_HSPC]

Project description:Analysis of MLLT3 genomic distribution and related chromatin features in uncultured fetal liver hematopoietic stem-progenitor cells [ChIPseq_FL_HSPC]

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RNA-seq of MLLT3-L and MLLT3-S overexpressing cultured HSPC, compared to non-overexpressing and uncultured FL-HSPC

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FLT3-N676K drives acute myeloid leukemia in a xenograft model of KMT2A-MLLT3 leukemogenesis

Project description:Activating signaling mutations are common in acute leukemia with KMT2A (previously MLL) rearrangements. Herein, we show that co-expression of FLT3-N676K and KMT2A-MLLT3 in human CD34+ cord blood cells primarily cause acute myeloid leukemia (AML) and rarely acute lymphoblastic leukemia (ALL) in immunodeficient mice. By contrast, expression of KMT2A-MLLT3 alone cause ALL, double-positive leukemia (DPL, expressing both CD33 and CD19), or bilineal leukemia (BLL, comprised of distinct myeloid and lymphoid leukemia cells), and rarely AML. Further, AML could only be serially propagated with maintained immunophenotype in secondary recipients when cells co-expressed KMT2A-MLLT3 and FLT3-N676K. Consistent with the idea that activated signaling would allow myeloid cells to engraft and maintain their self-renewal capacity, in a secondary recipient, a de novo KRAS-G13D was identified in myeloid cells previously expressing only KMT2A-MLLT3. Gene expression profiling revealed that KMT2A-MLLT3 DPL had a highly similar gene expression profile to ALL, with both expressing key lymphoid transcription factors and ALL cell surface markers, in line with the DPL cells being ALL cells with aberrant expression of CD33. Taken together, our results highlight the need for constitutive active signaling mutations for driving myeloid leukemia in a human xenograft model of KMT2A-R acute leukemia.

2019-04-05 | GSE127492 | GEO

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