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The MLL-Menin interaction is a molecular dependency in NUP98-rearranged AML

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE175597 | GEO | 2022/06/01

REPOSITORIES: GEO

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The MLL-Menin interaction is a molecular dependency in NUP98-rearranged AML [BioChIP-seq]

Project description:Using mouse and human models of NUP98-rearrranged leukemia, we demonstrate that inhibition of MLL-Menin impairs leukemogenic gene expression and disrupts chromatin binding of MLL1 and NUP98 fusion proteins at a critical subset of genes that is essential for sustaining the undifferentiated leukemia phenotype.

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The MLL-Menin interaction is a molecular dependency in NUP98-rearranged AML

Project description:The MLL-Menin interaction is a molecular dependency in NUP98-rearranged AML

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Project description:To investigate the effect of Menin inhibitor on patient-derived NUP98-r AML. We treated primary AML cells with Menin inhibitor in a Mesenchymal stem cell co-Culture platform. Then we charachterized global gene expression in treated AML cells upon treatment in two different time points, day7 and day12.

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The MLL-Menin interaction is a molecular dependency in NUP98-rearranged AML [ChIP-Seq]

Project description:The MLL-Menin interaction is a molecular dependency in NUP98-rearranged AML [ChIP-Seq]

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Molecular pathogenesis of disease progression in MLL-rearranged AML.

Project description:Leukemic relapse is frequently accompanied by progressively aggressive clinical course. To understand the molecular mechanism of leukemic relapse, MLL/AF9-transformed mouse leukemia cells were serially transplanted in C57BL/6 mice (N?=?96) by mimicking repeated recurrences, where mutations were monitored by exome sequencing (N = 42). The onset of leukemia was progressively promoted with advanced transplants, during which increasing numbers of somatic mutations were acquired (P?<?0.005). Among these, mutations in Ptpn11 (p.G60R) and Braf (p.V637E) corresponded to those identified in human MLL-AML, while recurrent mutations affecting Msn (p.R295C) were observed only in mouse but not in human MLL-AML. Another mutated gene of interest was Gnb2 which was reported to be recurrently mutated in various hematological neoplasms. Gnb2 mutations (p.G77R) were significantly increased in clone size (P?=?0.007) and associated with earlier leukemia onset (P?=?0.011). GNB2 transcripts were significantly upregulated in human MLL-AML compared to MLL-negative AML (P?<?0.05), which was supported by significantly increased Gnb2 transcript induced by MLL/AF9 overexpression (P?<?0.001). In in vivo model, both mutation and overexpression of GNB2 caused leukemogenesis, and downregulation of GNB2 expression reduced proliferative potential and survival benefit, suggesting a driver role of GNB2. In conclusion, alterations of driver genes over time may play an important role in the progression of MLL-AML.

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