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IDENTIFICATION AND FUNCTIONAL DEMONSTRATION OF A FETAL-SPECIFIC AXIS THAT POTENTLY SUPPRESSES MLL-FUSION DRIVEN MURINE AML miRNA-seq [L28BME vs ME]

ABSTRACT: IDENTIFICATION AND FUNCTIONAL DEMONSTRATION OF A FETAL-SPECIFIC AXIS THAT POTENTLY SUPPRESSES MLL-FUSION DRIVEN MURINE AML miRNA-seq [L28BME vs ME]

PROVIDER: PRJNA831204 | ENA |

REPOSITORIES: ENA

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IDENTIFICATION AND FUNCTIONAL DEMONSTRATION OF A FETAL-SPECIFIC AXIS THAT POTENTLY SUPPRESSES MLL-FUSION DRIVEN MURINE AML

Project description:IDENTIFICATION AND FUNCTIONAL DEMONSTRATION OF A FETAL-SPECIFIC AXIS THAT POTENTLY SUPPRESSES MLL-FUSION DRIVEN MURINE AML

| PRJNA828262 | ENA

IDENTIFICATION AND FUNCTIONAL DEMONSTRATION OF A FETAL-SPECIFIC AXIS THAT POTENTLY SUPPRESSES MLL-FUSION DRIVEN MURINE AML

Project description:MLL-rearrangements (MLL-r) are recurrent genetic events in acute myeloid leukemia (AML) and frequently associate with poor prognosis. In infants, MLL-r have been suggested to be sufficient to drive transformation. However, despite the prenatal origin of MLL-r, the incidence of congenital leukemia is very low with transformation usually occurring postnatally. The influence of prenatal signals on leukemogenesis, such as those mediated by the fetal-specific RNA binding protein LIN28B, remains controversial. Here, using a dual-transgenic mouse model that co-express MLL-ENL and LIN28B, we investigated the impact of LIN28B on AML. We show that LIN28B impedes the progression of MLL-r AML through a compromised leukemia initiating cell activity and a suppression of MYB signaling. Mechanistically, rather than involving the well-studied Lin28B-let7 miR axis, we found that LIN28B directly bound MYBBP1A mRNA, a co-repressor of MYB, and that positively correlated with MYBBP1A protein levels. Overexpression of MYBBP1A in MLL-ENL driven leukemogenesis largely phenocopied the tumor suppressor effects of LIN28B. Thereby, our work proposes that the developmentally-restricted expression of LIN28B during fetal development provides a protection against MYB-dependent AML.

2023-02-08 | GSE201083 | GEO

IDENTIFICATION AND FUNCTIONAL DEMONSTRATION OF A FETAL-SPECIFIC AXIS THAT POTENTLY SUPPRESSES MLL-FUSION DRIVEN MURINE AML RNA-seq [L28BME vs ME]

Project description:IDENTIFICATION AND FUNCTIONAL DEMONSTRATION OF A FETAL-SPECIFIC AXIS THAT POTENTLY SUPPRESSES MLL-FUSION DRIVEN MURINE AML RNA-seq [L28BME vs ME]

| PRJNA831156 | ENA

IDENTIFICATION AND FUNCTIONAL DEMONSTRATION OF A FETAL-SPECIFIC AXIS THAT POTENTLY SUPPRESSES MLL-FUSION DRIVEN MURINE AML miRNA-seq [WT vs ME]

Project description:IDENTIFICATION AND FUNCTIONAL DEMONSTRATION OF A FETAL-SPECIFIC AXIS THAT POTENTLY SUPPRESSES MLL-FUSION DRIVEN MURINE AML miRNA-seq [WT vs ME]

| PRJNA831177 | ENA

IDENTIFICATION AND FUNCTIONAL DEMONSTRATION OF A FETAL-SPECIFIC AXIS THAT POTENTLY SUPPRESSES MLL-FUSION DRIVEN MURINE AML miRNA-seq [WT vs ME]

Project description:LIN28B suppresses MLL-ENL driven AML. The tumor suppressor effects of LIN28B are largely driven by positive regulation of MYBBP1A.

2023-04-28 | GSE201371 | GEO

IDENTIFICATION AND FUNCTIONAL DEMONSTRATION OF A FETAL-SPECIFIC AXIS THAT POTENTLY SUPPRESSES MLL-FUSION DRIVEN MURINE AML RNA-seq [L28BME vs ME]

Project description:LIN28B suppresses MLL-ENL driven AML. The tumor suppressor effects of LIN28B are largely driven by positive regulation of MYBBP1A.

2023-04-28 | GSE201370 | GEO

IDENTIFICATION AND FUNCTIONAL DEMONSTRATION OF A FETAL-SPECIFIC AXIS THAT POTENTLY SUPPRESSES MLL-FUSION DRIVEN MURINE AML miRNA-seq [L28BME vs ME]

Project description:LIN28B suppresses MLL-ENL driven AML. The tumor suppressor effects of LIN28B are largely driven by positive regulation of MYBBP1A.

2023-04-28 | GSE201372 | GEO

Protein Interactions of 7 MLL-fusion Proteins

Project description:MLL-fusions represent a large group of leukemia drivers, whose diversity originates from the vast molecular heterogeneity of C-terminal fusion partners of MLL protein. While studies of selected MLL-fusions have revealed critical molecular pathways, unifying mechanisms across all MLL-fusions remain poorly understood. We present the first comprehensive survey of protein-protein interactions of seven distantly related MLL-fusion proteins: MLL-AF1p, MLL-AF4, MLL-AF9, MLL-CBP, MLL-EEN, MLL-ENL and MLL-GAS7.

2018-05-25 | PXD009338 | Pride

Identification of a Potently Oncogenic CALM-AF10 Minimal-Fusion Mutant

Project description:This SuperSeries is composed of the following subset Series: GSE27512: Identification of a Potently Oncogenic CALM-AF10 Minimal-Fusion Mutant (miRNA) GSE27513: Identification of a Potently Oncogenic CALM-AF10 Minimal-Fusion Mutant (mRNA) Refer to individual Series

2011-10-04 | E-GEOD-27514 | biostudies-arrayexpress

Menin-MLL inhibitors block oncogenic transformation by MLL fusion proteins in a fusion partner independent manner

Project description:Chromosomal rearrangements of the Mixed Lineage Leukemia (MLL) gene result in fusion proteins which retain the N-terminal portion of MLL fused with one of more than 70 different fusion partners. The high diversity of MLL fusion partners raises a question whether it is possible to develop a general therapeutic strategy to block the oncogenic activity of MLL fusion proteins in a fusion partner independent manner. We have demonstrated that blocking the menin-MLL interaction using small molecule inhibitor inhibits oncogenic activity of different MLL fusion proteins according to a mechanism that is independent on the fusion partner.

2018-06-09 | GSE69740 | GEO

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