Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Structural variants drive context dependent oncogene activation in cancer

ABSTRACT: Structural variants drive context dependent oncogene activation in cancer

PROVIDER: PRJNA613064 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other
	SRR11342200_1.fastq.gz	Fastqsanger.gz
	SRR11342200_2.fastq.gz	Fastqsanger.gz
	SRR11342300_1.fastq.gz	Fastqsanger.gz
	SRR11342300_2.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 627

Similar Datasets

Structural variants drive context dependent oncogene activation in cancer

Project description:Higher order chromatin structure is important for regulation of genes by distal regulatory sequences. Structural variants that alter 3D genome organization can lead to enhancer-promoter rewiring and human disease, particularly in the context of cancer. However, only a small minority of structural variants are associated with altered gene expression and it remains unclear why certain structural variants lead to changes in distal gene expression and others do not. To address these questions, we used a combination of genomic profiling and genome engineering to identify sites of recurrent changes in 3D genome structure in cancer and determine the effects of specific rearrangements on oncogene activation. By analyzing Hi-C data from 92 cancer cell lines and patient samples, we identified loci affected by recurrent alterations to 3D genome structure, including oncogenes such as MYC, TERT, and CCND1. Using CRISPR/Cas9 genome engineering to generate de novo structural variants, we show that oncogene activity can be predicted using “Activity-by-Contact” models that consider partner region chromatin contacts and enhancer activity. However, Activity-by-Contact models are only predictive of specific subsets of genes in the genome, suggesting that different classes of genes engage in distinct modes of regulation by distal regulatory elements. These results indicate that structural variants that alter 3D genome organization are widespread in cancer genomes and begin to illustrate predictive rules for the consequences of structural variants on oncogene activation.

2022-10-04 | GSE147123 | GEO

Structural variants drive context-dependent oncogene activation in cancer.

Project description:Higher-order chromatin structure is important for the regulation of genes by distal regulatory sequences1,2. Structural variants (SVs) that alter three-dimensional (3D) genome organization can lead to enhancer-promoter rewiring and human disease, particularly in the context of cancer3. However, only a small minority of SVs are associated with altered gene expression4,5, and it remains unclear why certain SVs lead to changes in distal gene expression and others do not. To address these questions, we used a combination of genomic profiling and genome engineering to identify sites of recurrent changes in 3D genome structure in cancer and determine the effects of specific rearrangements on oncogene activation. By analysing Hi-C data from 92 cancer cell lines and patient samples, we identified loci affected by recurrent alterations to 3D genome structure, including oncogenes such as MYC, TERT and CCND1. By using CRISPR-Cas9 genome engineering to generate de novo SVs, we show that oncogene activity can be predicted by using 'activity-by-contact' models that consider partner region chromatin contacts and enhancer activity. However, activity-by-contact models are only predictive of specific subsets of genes in the genome, suggesting that different classes of genes engage in distinct modes of regulation by distal regulatory elements. These results indicate that SVs that alter 3D genome organization are widespread in cancer genomes and begin to illustrate predictive rules for the consequences of SVs on oncogene activation.

| S-EPMC9810360 | biostudies-literature

Structural characterization of ribosome variants

Project description:Structural characterization of ribosome variants

| PRJNA414663 | ENA

3D genomic analysis reveals novel enhancer-hijacking caused by complex structural alterations that drive oncogene overexpression

Project description:3D genomic analysis reveals novel enhancer-hijacking caused by complex structural alterations that drive oncogene overexpression

| PRJNA949123 | ENA

ecDNA hubs drive cooperative intermolecular oncogene expression

Project description:ecDNA hubs drive cooperative intermolecular oncogene expression

| PRJNA671462 | ENA

ecDNA hubs drive cooperative intermolecular oncogene expression [HiChIP]

Project description:ecDNA hubs drive cooperative intermolecular oncogene expression [HiChIP]

| PRJNA671461 | ENA

ecDNA hubs drive cooperative intermolecular oncogene expression [ChIP]

Project description:ecDNA hubs drive cooperative intermolecular oncogene expression [ChIP]

| PRJNA671178 | ENA

Integrative Analysis of Pathogenic Structural Variants in Leukemia Genomes

Project description:Pathogenic Structural Variants in Leukemia Genomes