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Enhancer engagement sustains oncogenic transformation and progression of B-cell precursor acute lymphoblastic leukemia

ABSTRACT: Enhancer engagement sustains oncogenic transformation and progression of B-cell precursor acute lymphoblastic leukemia

PROVIDER: PRJNA887733 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21824300_1.fastq.gz	Fastqsanger.gz
	SRR21824300_2.fastq.gz	Fastqsanger.gz
	SRR21824301_1.fastq.gz	Fastqsanger.gz
	SRR21824301_2.fastq.gz	Fastqsanger.gz
	SRR21824302_1.fastq.gz	Fastqsanger.gz

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Enhancer engagement sustains oncogenic transformation and progression of B-cell precursor acute lymphoblastic leukemia

Project description:Numerous evidence report that non-genetic-driven events such as enhancer reprogramming promotes neoplastic transformation and strongly contribute to the phenotypical heterogeneity of cancers as much as genetic variation. In this study, we investigated the role of enhancers in sustaining oncogenic transformation in Paediatric B-cell Acute Lymphoblastic Leukemia (ALL-B), a type of cancer caused by the accumulation of lymphoid progenitor cells in the bone marrow.

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IL7R mutational activation can initiate Ph-like and PAX5 P80R precursor B-cell acute lymphoblastic leukemia

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-leukemia stage in which B-cell precursors display self-renewal ability, initiating precursor B-ALL that resembles PAX5 P80R or Ph-like human leukemia. 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 both 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 novel treatment avenues for IL-7R-related cases. Our model, a unique resource to explore the pathophysiology and therapeutic vulnerabilities of B-ALL, demonstrates that IL7R can initiate this malignancy.

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Human B-cell precursor acute lymphoblastic leukemia cells overexpressing ST6Gal1

Project description:Human B-cell precursor acute lymphoblastic leukemia cells overexpressing ST6Gal1

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Transcription profiling of human T-cell acute lymphoblastic leukemia, T-cell lymphoblastic lymphoma and B-precursor acute lymphoblastic leukemia samples

Project description:T-cell acute lymphoblastic leukemia (T-ALL) and T-cell lymphoblastic lymphoma (T-LL) and are often thought to represent a spectrum of a single disease. The malignant cells in T-ALL and T-LL are morphologically indistinguishable, and they share the expression of common cell surface antigens and cytogenetic characteristics. However, despite these similarities, differences in the predominant sites of disease in T-ALL and T-LL are observed. To determine if underlying biological distinctions may potentially contribute to some of these differences, we analyzed the global gene expression profiles of malignant T-cell precursors in ten T-ALL and nine T-LL using DNA arrays. Ten additional B-precursor ALL bone marrow samples, were used in a separate analysis. <br><br> Note that files GSM27087.txt and GSM27088.txt are identical as downloaded from GEO.

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Expression data from B-cell precursor acute lymphoblastic leukemia

Project description:B-cell precursor acute lymphoblastic leukemia (BCP-ALL) is a heterogeneous disease that can be subdivided according to primary recurrent genetic abnormalities that are strongly associated with characteristic biological and clinical features. The detection of these abnormalities can facilitate diagnosis, risk stratification, and targeted therapy. We identified an unexpectedly high incidence of fusion genes involving ZNF384 genes, including TCF3-ZNF384, EP300-ZNF384, and CREBBP-ZNF384, in BCP-ALL of our cohort. We therefore used microarrays to evaluate the gene-expression characteristics of BCP-ALL harboring ZNF384-related fusion genes and compared with those of BCP-ALL with other types of conventional genetic abnormality.

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Expression data of mesenchymal stromal cells after 40 hours of co-culture with primary B-cell precursor acute lymphoblastic leukemia cells

Project description:B-cell precursor acute lymphoblastic leukemia (BCP-ALL) cells reside in the bone marrow microenvironment, where they are protected against chemotherapeutic agents. Mesenchymal stromal cells (MSCs) are key components of this supporting framework. The present study aimed to unravel whether MSCs derived from pediatric BCP-ALL patients (leukemic MSCs) differ from MSCs derived from healthy pediatric donors (control-MSCs). Therefore, we studied their gene expression profiles after 40 hours of co-culture with primary B-cell precursor acute lymphoblastic leukemia cells. MSCs were sorted using fluorescence-activated cell sorting (FACS).

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Deregulated expression of cytokine receptor gene, CRLF2, is involved in lymphoid transformation in BCP-ALL

Project description:Deregulated expression of cytokine receptor gene, CRLF2, is involved in lymphoid transformation in B-cell precursor acute lymphoblastic leukemia We report two novel, cryptic chromosomal abnormalities in precursor B-cell acute lymphoblastic leukemia (BCP-ALL): a translocation, either t(X;14)(p22;q32) or t(Y;14)(p11;q32), in 33 patients and an interstitial deletion, either del(X)(p22.33p22.33) or del(Y)(p11.32p11.32), in 64 patients, involving the pseudoautosomal region (PAR1) of the sex chromosomes. The incidence of these abnormalities was 5% in childhood ALL (0.8% with the translocation, 4.2% with the deletion). Patients with the translocation were older (median age 16 years), whilst the patients with the deletion were younger (median age 4 years). The two abnormalities result in deregulated expression of the cytokine receptor, cytokine receptor-like factor 2, CRLF2 (also known as thymic stromal-derived lymphopoietin receptor, TSLPR). Over-expression of CRLF2 was associated with activation of the JAK-STAT pathway in cell lines and transduced primary B-cell progenitors, sustaining their proliferation and indicating a causal role of CRLF2 over-expression in lymphoid transformation. In Down Syndrome (DS) ALL and two non DS BCP-ALL cell lines, CRLF2 deregulation was associated with mutations of the JAK2 pseudokinase domain suggesting oncogenic cooperation, as well as highlighting a link between non DS ALL and JAK2 mutations. Keyword(s): Global copy number analysis using Agilent oligonucleotide arrays DNA copy number analysis of 16 acute lymphoblastic leukaemia samples (13 diagnostic, 1 diagnostic and relapse pair and 2 cell-lines) was performed using Agilent 244K and 105K custom microarrays. These samples were hybridised against gender matched reference DNA.

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Project description:miR-126 Orchestrates an Oncogenic Program in B-Cell Precursor Acute Lymphoblastic Leukemia

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