Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

TET2 deficiency subverts tumor immunity [model 3]

ABSTRACT: TET2 deficiency subverts tumor immunity [model 3]

PROVIDER: PRJNA851067 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR19754328.fastq.gz	Fastqsanger.gz
	SRR19754329.fastq.gz	Fastqsanger.gz
	SRR19754330.fastq.gz	Fastqsanger.gz
	SRR19754331.fastq.gz	Fastqsanger.gz

Items per page:

1 - 4 of 4

Similar Datasets

TET2 deficiency subverts tumor immunity [model 3]

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 | GSE206487 | GEO

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]

| PRJNA851019 | ENA

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]

| PRJNA851020 | ENA

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

2023-06-23 | GSE206456 | GEO

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

2023-06-23 | GSE206457 | GEO

TET2 deficiency

Project description:TET2 deficiency

| PRJNA851062 | ENA

TET2-mediated mRNA in tumor immunity [m5C]

Project description:TET2-mediated mRNA in tumor immunity [m5C]

| PRJNA963841 | ENA

B-cell tumor development in Tet2-deficient mice

Project description:The TET2 gene encodes an α-ketoglutarate-dependent dioxygenase able to oxidize 5-methylcytosine into 5-hydroxymethylcytosine, which is a step toward active DNA demethylation. TET2 is frequently mutated in myeloid malignancies but also in B- and T-cell malignancies. TET2 somatic mutations are also identified in healthy elderly individuals with clonal hematopoiesis. Tet2-deficient mouse models showed widespread hematological differentiation abnormalities, including myeloid, T-cell, and B-cell malignancies. We show here that, similar to what is observed with constitutive Tet2-deficient mice, B-cell-specific Tet2 knockout leads to abnormalities in the B1-cell subset and a development of B-cell malignancies after long latency. Aging Tet2-deficient mice accumulate clonal CD19+ B220low immunoglobulin M+ B-cell populations with transplantable ability showing similarities to human chronic lymphocytic leukemia, including CD5 expression and sensitivity to ibrutinib-mediated B-cell receptor (BCR) signaling inhibition. Exome sequencing of Tet2-/- malignant B cells reveals C-to-T and G-to-A mutations that lie within single-stranded DNA-specific activation-induced deaminase (AID)/APOBEC (apolipoprotein B messenger RNA editing enzyme, catalytic polypeptide-like) cytidine deaminases targeted motif, as confirmed by the lack of a B-cell tumor in compound Tet2-Aicda-deficient mice. Finally, we show that Tet2 deficiency accelerates and exacerbates T-cell leukemia/lymphoma 1A-induced leukemogenesis. Together, our data establish that Tet2 deficiency predisposes to mature B-cell malignancies, which development might be attributed in part to AID-mediated accumulating mutations and BCR-mediated signaling. This accession concerns 46 transcriptomic experiments with Affymetrix Mouse 430-2 array..

2019-12-12 | E-MTAB-8501 | biostudies-arrayexpress

TET2 promotes anti-tumor immunity by governing G-MDSCs and CD8+ T cell numbers

Project description:Host immune response is a fundamental mechanism for attenuating cancer progression. Here we report a pivotal role of the DNA demethylase and tumor suppressor TET2 played in host antitumor immunity. Deletion of Tet2 dramatically elevated the IL-6 level in Tet2-/- mice upon tumor challenge. The elevated IL-6 greatly stimulated the immunosuppressive granulocytic myeloid-derived suppressor cells (G-MDSCs), which in turn significantly reduced CD8+ T cells upon tumor challenge. Consequently, systematic knockout of the Tet2 in mice led to accelerated syngeneic tumor growth, which was constrained by anti-PD-1 blockade. Removal of G-MDSCs by the anti-mouse Ly6g Ab restored the numbers of CD8+ T cells in Tet2-/- mice and rebooted their anti-tumor activity. Importantly, anti-IL-6 Ab treatment blocked the expansion of G-MDSCs and inhibited syngeneic tumor growth. Collectively, these findings reveal a TET2-mediated IL-6/G-MDSC/CD8+ T immune response cascade that safeguards host adaptive anti-tumor immunity, offering a cell non-autonomous mechanism of TET2 for tumor suppression.

2020-08-04 | GSE144787 | GEO

TET2 deficiency promotes MDS-associated leukemogenesis

Project description:TET2 deficiency promotes MDS-associated leukemogenesis

| PRJNA881305 | ENA