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An instructive role for Interleukin-7 receptor α in the development of human B-cell precursor leukemia

ABSTRACT: Bulk RNAseq for transplanted transduced (CRLF2-IL7RAins or BB control)CB cells

ORGANISM(S): Homo sapiens

PROVIDER: GSE190070 | GEO | 2021/12/06

REPOSITORIES: GEO

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An instructive role for Interleukin-7 receptor α in the development of human B-cell precursor leukemia

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Project description:There are two samples, 42 (control) and 49 To test the role of activated CRLF2/IL7RA in leukemia initiation we expressed CRLF2 together with IL7RA in human CB hematopoietic progenitors. Human CRLF2 and wild type and/or activated mutant form of human IL7RA (IL7RAwt/ins) were cloned into a lentiviral vector with a bi-cistronic cassette under the expression control of an EÃŽÂ¼-B29 promoter/enhancer to augment expression in B-cell precursors. Backbone vector expressing GFP (BB). Whole genome sequencing Leukemic (49) and BB transduced (42) corresponding CB cells were collected from transplanted mice. Sequencing libraries were prepared from these samples

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An instructive role for IL7RA in the development of human B-cell precursor leukemia

Project description:10X single cell analysis of human leukemia, pre-leukemia and normal control. The leukemia was developed in xenograft mice that was serialy transplanted with cells from primary mouse that was transplanted with normal cord blood after transduction with virues encoding hyper activated mutant IL7RA. The preleukemic cells are from the primary engrafted mouse and the control is the same cord blood that was transduced with backbone virus expressing GFP.

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Project description:Interleukin-7 receptor α (encoded by IL7R) is essential for lymphoid development. Whether acute lymphoblastic leukemia (ALL)-related IL7R gain-of-function mutations can trigger leukemogenesis remains unclear. Here, we demonstrate that lymphoid-restricted mutant IL7R, expressed at physiological levels in conditional knock-in mice, establishes a pre-leukemic stage in which B-cell precursors display self-renewal ability, initiating leukemia resembling PAX5 P80R or Ph-like human B-ALL. Full transformation associates with transcriptional upregulation of oncogenes such as Myc or Bcl2, downregulation of tumor suppressors such as Ikzf1 or Arid2, and major IL-7R signaling upregulation (involving JAK/STAT5 and PI3K/mTOR), required for leukemia cell viability. Accordingly, maximal signaling drives full penetrance and early leukemia onset in homozygous IL7R mutant animals. Notably, we identify 2 transcriptional subgroups in mouse and human Ph-like ALL, and show that dactolisib and sphingosine-kinase inhibitors are potential treatment avenues for IL-7R-related cases. Our model, a resource to explore the pathophysiology and therapeutic vulnerabilities of B-ALL, demonstrates that IL7R can initiate this malignancy.

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An instructive role for Interleukin-7 receptor α in the development of human B-cell precursor leukemia

Project description:An instructive role for Interleukin-7 receptor α in the development of human B-cell precursor leukemia

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An instructive role for IL7RA in the development of human B-cell precursor leukemia

Project description:Kinase signaling fuels growth of B-cell precursor acute lymphoblastic leukemia (BCP-ALL). Yet its role in leukemia initiation is unclear and has not been shown in primary human hematopoietic cells. We previously described activating mutations in interleukin-7 receptor alpha (IL7RA) in poor-prognosis Ã¢Â€Âœph-likeÃ¢Â€Â BCP-ALL. Here we show that expression of activated mutant IL7RA in human CD34+ hematopoietic cells creates a preleukemic state in transplanted NOD/LtSz-scid IL2RÃŽÂ³null mice, characterized by persistence of self-renewing Pro-B cells with non-productive V(D)J gene rearrangements. Preleukemic CD34+CD10highCD19+ cells evolved to a BCP-ALL with spontaneously acquired CDKN2A deletions as commonly observed in primary human BCP-ALL. CRISPR mediated silencing of CDKN2A in primary human CD34+ cells transduced with activated IL7RA resulted in robust development of BCP-ALLs in-vivo. Thus, we demonstrate for the first time that constitutive activation of IL7RA can initiate preleukemia in primary human hematopoietic progenitors and cooperates with CDKN2A silencing in progression into BCP-ALL.

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CRLF2 Over-expression is a Poor Prognostic Marker in Children With High Risk T-Cell Acute Lymphoblastic Leukemia

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