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Intrinsic Protection From Leukemic Transformation at The Level of Hematopoietic Stem Cells

ABSTRACT: Genome wide RNA-seq from pGM and HSCs in response to expression of the MLL-ENL fusion gene

ORGANISM(S): Mus musculus

PROVIDER: GSE62734 | GEO | 2015/01/01

SECONDARY ACCESSION(S): PRJNA265042

REPOSITORIES: GEO

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Intrinsic Protection From Leukemic Transformation at The Level of Hematopoietic Stem Cells

Project description:Genome wide RNA-seq from pGM and HSCs in response to expression of the MLL-ENL fusion gene Examination of mRNA abundance in two cell types with or without induction of the MLL-ENL fusion gene (following 48h of culture)

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Gene expression profiling of ST-HSCs and MPP2 cells conditionally expressing MLL-ENL by RNA-seq

Project description:To investigate the molecular mechanism of leukemic transformation by MLL-ENL in HSCs and immature progenitors, we preliminarily performed comprehensive gene expression profiling of ST-HSCs and MPP2 cells by RNA-seq using a mouse model enabling to conditionally express MLL-ENL at an endogenous-like expression level.

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Gene expression profiling of LT-HSCs and ST-HSCs conditionally expressing MLL-ENL

Project description:We have developed a new conditional transgenic mouse showing that MLL-ENL, at an endogenous-like expression level, induces leukemic transformation selectively in LT-HSCs. To investigate the molecular mechanism of leukemic transformation in LT-HSCs conditionally expressing MLL-ENL, we preliminarily performed comprehensive gene expression profiling of CreER-transduced LT-HSCs and ST-HSCs using cDNA microarray analysis. For initial screening of candidate genes invloved in the leukemic transformation, total RNA was extracted from colony-forming cells derived from LT-HSCs and ST-HSCs transduced with CreER or mock. Four samples were analyzed, and CreER-transduced LT/ST-HSC-derived cells were compared with mock-transduced LT/ST-HSC-derived cells, while CreER/mock-transduced LT-HSC-derived cells were compared with CreER/mock-transduced ST-HSC-derived cells.

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Heritable fetal protection against MLL::ENL-driven leukemogenesis depends on MLL3 [scATAC-seq]

Project description:MLL rearrangements (MLLr) are the most common cause of congenital and infant leukemias. MLLr arise prior to birth and require very few cooperating mutations for transformation, yet congenital leukemias are 10-fold less common than infant leukemias and >100-fold less common than childhood leukemias overall. This raises the question of whether mechanisms exist to suppress leukemic transformation during fetal life. Here, we show that in mice, fetal MLL::ENL exposure creates a heritable, leukemia-resistant state. MLL::ENL imposes a negative selective pressure on fetal hematopoietic progenitors that persists after birth to suppress transformation. These changes do not occur when MLL::ENL is induced shortly after birth, and transformation proceeds efficiently in that context. The fetal barrier to transformation is enforced by MLL3. It can be bypassed by cooperating mutations or inactivation of MLL3. Heritable, fetal protection against leukemic transformation may explain the low incidence of congenital leukemias in humans despite prenatal MLL rearrangement.

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