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Enforcement of stem-cell dormancy by NPMc+ is a critical determinant of unrestricted self-renewal during myeloid leukemogenesis

ABSTRACT: Analysis of the transcriptional profile imposed by NPMc+ and Flt3-ITD oncogenes, both alone and in cooperation, on HSCs at single cell level

ORGANISM(S): Mus musculus

PROVIDER: GSE133080 | GEO | 2025/03/01

REPOSITORIES: GEO

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Enforcement of stem-cell dormancy by NPMc+ is a critical determinant of unrestricted self-renewal during myeloid leukemogenesis

Project description:Purpose: Analysis of downstream pathways activated by NPMc+ and Flt3-ITD oncogenes in preleukemic hematopoietic stem cells (HSCs). Methods: RNA extracted and processed from MxCRE, Flt3-ITD and NPMc+/Flt3-ITD FACS sorted HSCs Results: These data demonstrate that NPMc+ expression in Flt3-ITD HSCs promote a transcriptional program that supports both self-renewal and quiescence.

2025-03-01 | GSE133077 | GEO

Enforcement of stem-cell dormancy by nucleophosmin mutation is a critical determinant of unrestricted self-renewal during myeloid leukemogenesis

Project description:The most frequent mutation in AML patients with normal karyotype affects the Nucleophosmin gene (NPMc+). Different mouse models have shown that NPMc+ mutation can drive leukemia development. In this study, the impact of NPMc+ expression on the transcriptional program of mouse hematopietic stem cells (HSC) in vivo has been investigated.

2025-02-28 | GSE94650 | GEO

Enforcement of stem-cell dormancy by NPMc+ is a critical determinant of unrestricted self-renewal during myeloid leukemogenesis

Project description:This SuperSeries is composed of the SubSeries listed below.

2025-03-01 | GSE133081 | GEO

Enforcement of stem-cell dormancy by NPMc+ is a critical determinant of unrestricted self-renewal during myeloid leukemogenesis

Project description:Enforcement of stem-cell dormancy by NPMc+ is a critical determinant of unrestricted self-renewal during myeloid leukemogenesis

| PRJNA549913 | ENA

Enforcement of stem-cell dormancy by NPMc+ is a critical determinant of unrestricted self-renewal during myeloid leukemogenesis

Project description:Enforcement of stem-cell dormancy by NPMc+ is a critical determinant of unrestricted self-renewal during myeloid leukemogenesis

| PRJNA549914 | ENA

Enforcement of stem-cell dormancy by NPMc+ is a critical determinant of unrestricted self-renewal during myeloid leukemogenesis

Project description:Enforcement of stem-cell dormancy by NPMc+ is a critical determinant of unrestricted self-renewal during myeloid leukemogenesis

| PRJNA549886 | ENA

MicroRNA profiling of human acute myeloid leukemia samples from patients characterized for subcellular localization/mutation status of NPM1 and FLT3 mutations

Project description:Acute myeloid leukemia (AML) carrying NPM1 mutations and cytoplasmic nucleophosmin (NPMc+ AML) accounts for about one-third of adult AML and shows distinct features, including a unique gene expression profile. MicroRNAs (miRNAs) are small noncoding RNAs of 19-25 nucleotides in length that have been linked to the development of cancer. Here, we investigated the role of miRNAs in the biology of NPMc+ AML. The miRNA expression was evaluated in 85 adult de novo AML patients characterized for subcellular localization/mutation status of NPM1 and FLT3 mutations using a custom microarray platform. Data were analyzed by using univariate t test within BRB tools. We identified a strong miRNA signature that distinguishes NPMc+ mutated (n = 55) from the cytoplasmic-negative (NPM1 unmutated) cases (n = 30) and includes the up-regulation of miR-10a, miR-10b, several let-7 and miR-29 family members. Many of the down-regulated miRNAs including miR-204 and miR-128a are predicted to target several HOX genes. Indeed, we confirmed that miR-204 targets HOXA10 and MEIS1, suggesting that the HOX up-regulation observed in NPMc+ AML may be due in part by loss of HOX regulators-miRNAs. FLT3-ITD+ samples were characterized by up-regulation of miR-155. Further experiments demonstrated that the up-regulation of miR-155 was independent from FLT3 signaling. Our results identify a unique miRNA signature associated with NPMc+ AML and provide evidence that support a role for miRNAs in the regulation of HOX genes in this leukemia subtype. Moreover, we found that miR-155 was strongly but independently associated with FLT3-ITD mutations.

2008-03-14 | E-TABM-429 | biostudies-arrayexpress

RIPK3 restricts myeloid leukemogenesis by promoting cell death and differentiation of leukemia initiating cells

Project description:Examination of gene expression patterns in lineage negative FLT3-ITDâ and pMIG-transduced BM cells via microarray study. We performed a global mRNA profiling analysis of murine Linâ FLT3-ITD+ cells compared to empty-vector controls, purified 48h after transduction. We examined association patterns of FLT3-ITD and pMIG cells and identified a specific gene expression signature associated with FLT3-ITD signalling. Total RNA obtained from isolated lineage negative BM cells subjected to 48h of FLT3-ITD signalling compared to empty vector control.

2016-08-22 | E-GEOD-79040 | biostudies-arrayexpress

RIPK3 restricts myeloid leukemogenesis by promoting cell death and differentiation of leukemia initiating cells

Project description:Examination of gene expression patterns in lineage negative FLT3-ITD– and pMIG-transduced BM cells via microarray study. We performed a global mRNA profiling analysis of murine Lin– FLT3-ITD+ cells compared to empty-vector controls, purified 48h after transduction. We examined association patterns of FLT3-ITD and pMIG cells and identified a specific gene expression signature associated with FLT3-ITD signalling.

2016-08-22 | GSE79040 | GEO

Alkynyl nicotinamides with antileukemic activity to treat poor prognosis AM

Project description:FLT3 activating mutations cause myeloproliferative neoplasms by deregulating hematopoietic progenitor cell growth, and acute myeloid leukemia is on the rise. Investigational drugs targeting mutant FLT3, including Quizartinib and Crenolanib, develop inherent and acquired resistance to FLT3 targeted therapy. FLT3 inhibitor resistance in AML is dependent on co-occurring mutations, parallel survival pathways, and/or subsequent FLT3-ITD mutations. Despite the high prevalence of FLT3 mutations and their clinical significance in AML, there are few targeted therapeutic options. We identified two novel naphthyridine-based FLT3 inhibitors (HSN608 and HSN748) that specifically target FLT3-ITD at sub-nanomolar concentrations and are effective against drug-resistant secondary mutations. In the current study, we evaluated these compounds antileukemic activity against FLT3-ITD and gatekeeper mutations in drug-resistant AML, relapsed/refractory AMLs with FLT3 mutations, and in vivo mouse models with combinations of epigenetic mutations TET2 with FLT3-ITD, and AML patients PDX. In these model systems, we demonstrate that HSN748 outperforms the FDA-approved FLT3 inhibitor Gilteritinib in terms of inhibitory activity against FLT3-ITD.

2022-12-07 | MSV000090855 | MassIVE

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