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EZH2 mutations reprogram the immune response to yield a pre-malignant lymphoma niche [ChIP-Seq]

ABSTRACT: EZH2 mutations reprogram the immune response to yield a pre-malignant lymphoma niche [ChIP-Seq]

PROVIDER: PRJNA574277 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10189246.fastq.gz	Fastqsanger.gz
	SRR10189247.fastq.gz	Fastqsanger.gz
	SRR10189248.fastq.gz	Fastqsanger.gz
	SRR10189249.fastq.gz	Fastqsanger.gz
	SRR10189250.fastq.gz	Fastqsanger.gz

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EZH2 mutations reprogram the immune response to yield a pre-malignant lymphoma niche

Project description:EZH2 mutations reprogram the immune response to yield a pre-malignant lymphoma niche

| PRJNA574275 | ENA

EZH2 mutations reprogram the immune response to yield a pre-malignant lymphoma niche [RNA-Seq]

Project description:EZH2 mutations reprogram the immune response to yield a pre-malignant lymphoma niche [RNA-Seq]

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EZH2 mutations reprogram the immune response to yield a pre-malignant lymphoma niche [Single cell RNA-Seq (10X Genomics)]

Project description:EZH2 mutations reprogram the immune response to yield a pre-malignant lymphoma niche [Single cell RNA-Seq (10X Genomics)]

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EZH2 mutations reprogram the immune response to yield a pre-malignant lymphoma niche [RNA-Seq]

Project description:The mechanism through which lymphoma-associated EZH2 gain-of-function mutations disrupt the immune system to initiate malignant transformation is poorly understood. Conditional expression of mutant Ezh2 in germinal center (GC) B-cells provides a competitive advantage to activated B-cells in expanding the GC light zone (LZ) that is not caused by failure to differentiate and exit the GC. Instead, the LZ enlargement is explained by reduced apoptosis of Ezh2 mutant centrocytes, aberrant LZ proliferation, and failure of these centrocytes to re-enter the dark zone (DZ). Ezh2 mutant GCs fail to engage T-cells and to undergo clonal diversification, exhibiting a reduced IgV mutation frequency. Hence the dominant competitive advantage effect of Ezh2 mutation during early stages of transformation is to uncouple GC B-cells from T-cell help checkpoint, which allows GC B-cells entering the LZ to persist and expand regardless of their immunoglobulin status, reflecting the biology of low-grade follicular lymphomas.

2020-05-11 | GSE138032 | GEO

EZH2 mutations reprogram the immune response to yield a pre-malignant lymphoma niche [ChIP-Seq]

2020-05-11 | GSE138036 | GEO

EZH2 mutations reprogram the immune response to yield a pre-malignant lymphoma niche [Single cell RNA-Seq (10X Genomics)]

2020-05-11 | GSE138033 | GEO

EZH2 mutations reprogram the immune response to yield a pre-malignant lymphoma niche

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

2020-05-11 | GSE138037 | GEO

Reprogram-seq

Project description:Reprogram-seq

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Affinify Purification of EZH2 and phosphodeficient EZH2 identifies phosphorylation dependent interactions of EZH2

Project description:Overexpression of EZH2 in estrogen receptor negative (ER-) breast cancer promotes metastasis. EZH2 has been mainly studied as the catalytic component of the Polycomb Repressive Complex 2 (PRC2) that mediates gene repression by trimethylating histone H3 at lysine 27 (H3K27me3). However, how EZH2 drives metastasis despite the low H3K27me3 levels observed in ER- breast cancer is unknown. We have shown that in human invasive carcinomas and distant metastases, cytoplasmic EZH2 phosphorylated at T367 is significantly associated with ER- disease and low H3K27me3 levels. Here, we explore the interactome of EZH2 and of a phosphodeficient mutant EZH2_T367A. We identified novel interactors of EZH2, and identified interactions that are dependent on the phosphorylation and cellular localization of EZH2 that may play a role in EZH2 dependent metastatic progression.

2018-07-03 | PXD010073 | Pride

Tanshinone I inhibit normal and malignant hematopoiesis by repressing EZH2 activity

Project description:Tanshinone I inhibit normal and malignant hematopoiesis by repressing EZH2 activity

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