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CRISPR screens identify gene targets at breast cancer risk loci [HiChIP]

ABSTRACT: CRISPR screens identify gene targets at breast cancer risk loci [HiChIP]

PROVIDER: PRJNA907300 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22486293_1.fastq.gz	Fastqsanger.gz
	SRR22486293_2.fastq.gz	Fastqsanger.gz
	SRR22486294_1.fastq.gz	Fastqsanger.gz
	SRR22486294_2.fastq.gz	Fastqsanger.gz
	SRR22486295_1.fastq.gz	Fastqsanger.gz

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CRISPR screens identify gene targets at breast cancer risk loci [HiChIP]

Project description:Genome-wide association studies (GWAS) have identified >200 loci associated with breast cancer (BC) risk. The majority of candidate causal variants (CCVs) are in non-coding regions and likely modulate cancer risk by regulating gene expression. However, pinpointing the exact target of the association, and identifying the phenotype it mediates, is a major challenge in the interpretation and translation of GWAS.

2023-03-09 | GSE219164 | GEO

CRISPR screens identify gene targets at breast cancer risk loci

Project description:CRISPR screens identify gene targets at breast cancer risk loci

| PRJNA907296 | ENA

CRISPR screens identify gene targets at breast cancer risk loci [RNA-seq]

Project description:CRISPR screens identify gene targets at breast cancer risk loci [RNA-seq]

| PRJNA907298 | ENA

CRISPR screens identify gene targets at breast cancer risk loci [ATAC-seq]

Project description:CRISPR screens identify gene targets at breast cancer risk loci [ATAC-seq]

| PRJNA907301 | ENA

CRISPR screens identify gene targets at breast cancer risk loci.

Project description:BackgroundGenome-wide association studies (GWAS) have identified > 200 loci associated with breast cancer risk. The majority of candidate causal variants are in non-coding regions and likely modulate cancer risk by regulating gene expression. However, pinpointing the exact target of the association, and identifying the phenotype it mediates, is a major challenge in the interpretation and translation of GWAS.ResultsHere, we show that pooled CRISPR screens are highly effective at identifying GWAS target genes and defining the cancer phenotypes they mediate. Following CRISPR mediated gene activation or suppression, we measure proliferation in 2D, 3D, and in immune-deficient mice, as well as the effect on DNA repair. We perform 60 CRISPR screens and identify 20 genes predicted with high confidence to be GWAS targets that promote cancer by driving proliferation or modulating the DNA damage response in breast cells. We validate the regulation of a subset of these genes by breast cancer risk variants.ConclusionsWe demonstrate that phenotypic CRISPR screens can accurately pinpoint the gene target of a risk locus. In addition to defining gene targets of risk loci associated with increased breast cancer risk, we provide a platform for identifying gene targets and phenotypes mediated by risk variants.

| S-EPMC10053147 | biostudies-literature

CRISPR screens identify gene targets at breast cancer risk loci [ATAC-seq]

2023-03-09 | GSE219163 | GEO

CRISPR screens identify gene targets at breast cancer risk loci [RNA-seq]

2023-03-09 | GSE219166 | GEO

CRISPR screens identify gene targets at breast cancer risk loci

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

2023-03-08 | GSE219168 | GEO

CRISPR-based epigenome editing screens identify transcriptional and epigenetic regulators of human CD8 T cell function [Sorting-based CRISPR screens]

Project description:All bulk CRISPR based screens CD2 and B2M CRISPRi tiling screens (primary human CD8 T cells), IL2RA CRISPRa tiling screens (Jurkats), CRISPRi/a TF screens (primary human CD8 T cells), and CRISPR TFome KO (primary human T cells)

2023-08-31 | GSE241933 | GEO

Analysis of promoter-associated chromatin interactions reveals biologically relevant candidate target genes at endometrial cancer risk loci

Project description:The identification of target genes at genome-wide association study (GWAS) loci is a major obstacle for GWAS follow-up. To identify candidate target genes at the 16 known endometrial cancer GWAS risk loci, we performed HiChIP chromatin looping analysis of endometrial cell lines. To enrich for enhancer-promoter interactions, a mechanism through which GWAS variation may target genes, we captured loops associated with H3K27Ac histone, characteristic of promoters and enhancers. Analysis of HiChIP loops contacting promoters revealed enrichment for endometrial cancer GWAS heritability and intersection with endometrial cancer risk variation identified 103 HiChIP target genes at 13 risk loci. Expression of four HiChIP target genes (SNX11, SRP14, HOXB2 and BCL11A) was associated with risk variation, providing further evidence for their regulation. Network analysis functionally prioritized a set of proteins that interact with those encoded by HiChIP target genes, and this set was enriched for pan-cancer and endometrial cancer drivers. Lastly, HiChIP target genes and prioritized interacting proteins were over-represented in pathways related to endometrial cancer development. In summary, we have generated the first global chromatin looping data from endometrial cells, enabling analysis of all known endometrial cancer risk loci and identifying biologically relevant candidate target genes.

2020-04-13 | GSE137936 | GEO

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