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TET2 deficiency maintains leukemia stem cell self-renewal and subverts tumor immunity [model 2]

ABSTRACT: To investigate the function of TET2 in the development of acute myeloid leukemia (AML), we performed gene expression profiling analysis using data obtained from RNA-seq of AML cells carrying Tet2+/+ versus Tet2-/-.

ORGANISM(S): Mus musculus

PROVIDER: GSE206457 | GEO | 2023/06/23

REPOSITORIES: GEO

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TET2 deficiency maintains leukemia stem cell self-renewal and subverts tumor immunity [model 1]

Project description:To investigate the function of TET2 in the development of acute myeloid leukemia (AML), we performed gene expression profiling analysis using data obtained from RNA-seq of AML cells carrying Tet2+/+ versus Tet2-/-.

2023-06-23 | GSE206456 | GEO

TET2 deficiency subverts tumor immunity [model 3]

2023-06-23 | GSE206487 | GEO

TET2 deficiency maintains leukemia stem cell self-renewal and subverts tumor immunity [model 1]

Project description:TET2 deficiency maintains leukemia stem cell self-renewal and subverts tumor immunity [model 1]

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TET2 deficiency maintains leukemia stem cell self-renewal and subverts tumor immunity [model 2]

Project description:TET2 deficiency maintains leukemia stem cell self-renewal and subverts tumor immunity [model 2]

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TET2-mediated mRNA in tumor immunity [m5C]

Project description:To investigate the function of TET2 as an mRNA m5C demethylase in the development of acute myeloid leukemia (AML), we conducted RNA bisulfite sequencing of mRNA samples enriched from AML cells carrying Tet2+/+ versus Tet2-/- with actinomycin D treatment at different time point.

2023-06-23 | GSE231329 | GEO

TET2 deficiency subverts tumor immunity [model 3]

Project description:TET2 deficiency subverts tumor immunity [model 3]

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Tet2 loss leads to increased hematopoietic stem cell self-renewal and myeloid transformation

Project description:Recurrent somatic mutations in TET2 and in other genes that regulate the epigenetic state have been identified in patients with myeloid malignancies and in other cancers. However, the in vivo effects of Tet2 loss have not been delineated. We report here that Tet2 loss leads to increased stem-cell self-renewal and to progressive stem cell expansion. Consistent with human mutational data, Tet2 loss leads to myeloproliferation in vivo, notable for splenomegaly and monocytic proliferation. In addition, haploinsufficiency for Tet2 confers increased self-renewal and myeloproliferation, suggesting that the monoallelic TET2 mutations found in most TET2-mutant leukemia patients contribute to myeloid transformation. This work demonstrates that absent or reduced Tet2 function leads to enhanced stem cell function in vivo and to myeloid transformation. These studies show that a ubiquitin ligase-substrate pair can orchestrate the molecular program of HSC differentitiation Gene expression profiles from WT and Tet2-/- sorted LSK and myeloid progenitors (CMP and GMP) were compared using genome wide mRNA expression profiling by Affymetrix genechip arrays (Mouse 430 2.0) and key targets were validated by chromatin immunoprecipitation experiments.

2011-07-01 | E-GEOD-27816 | biostudies-arrayexpress

TET2 deficiency

Project description:TET2 deficiency

| PRJNA851062 | ENA

Tet2 loss leads to increased hematopoietic stem cell self-renewal and myeloid transformation

2011-07-01 | GSE27816 | GEO

TP53 loss and TET2 deficiency cooperate to drive lineage-plastic leukemogenesis by transforming progenitors and establishing immune suppressive environment

Project description:Loss-of-function mutations of TET2 and TP53 genes are frequently co-observed in AML patients receiving intensive chemotherapy and represent independent predictors for inferior survival in patients after stem cell transplantation. Here we show that TET2 biallelic loss or haploinsufficiency is observed in >10% AML patients with TP53 mutations and associated with poor outcome. In mice, double deletions of TET2 and P53 leads to development of T-ALL, B-ALL or AML and stimulation of pre-leukemic mice via TLR2-TRAF6-A20 axis skews leukemia development toward AML. scRNA-seq of murine blasts reveals that B cell leukemia differentiation is accompanied by transcriptional changes of ll7r and Myb while AML commitment is associated with dynamic elevation of Klf4 and Flt3. Notably, mice with AML exhibit T cell exhaustion, NK dysfunction, and MDSC-like properties which are similarly observed in AML patients with TP53/TET2 co-mutations. Lastly, we demonstrated that silencing of MEK/ERK, JAK/STAT or TLR-A20 signaling pathways, that are overexpressed in TP53/TET2-mutant AML, restores normal differentiation in vitro and in vivo. Collectively, these findings provide evidence that TP53 deficiency and TET2 loss cooperate to transform hematopoietic progenitors and play a role in AML development and identify novel targets to deliver therapy for this high-risk AML group.

2023-11-13 | GSE217867 | GEO

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