Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Tumor model generation by somatic Cas9-mediated tumor suppressor gene disruption

ABSTRACT: Tumor model generation by somatic Cas9-mediated tumor suppressor gene disruption

PROVIDER: PRJEB6541 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	ERR538012_1.fastq.gz	Fastqsanger.gz
	ERR538012_2.fastq.gz	Fastqsanger.gz
	ERR538013_1.fastq.gz	Fastqsanger.gz
	ERR538013_2.fastq.gz	Fastqsanger.gz
	ERR538014_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 46

Similar Datasets

Somatic CRISPR/Cas9-mediated tumor suppressor disruption enables versatile murine cancer modeling

Project description:Recent cancer genome sequencing studies have identified numerous novel candidate driver genes. In vivo functional investigation of oncogenes using somatic gene transfer has been successfully exploited as a versatile means to validate their pathogenic relevance. In contrast, such functional analyses have been hampered for candidate tumor suppressor genes, e.g. by insufficient knockdown using RNAi-mediated approaches. In order to provide a flexible method for investigating loss-of-function mutations and their potential role in tumorigenesis, we have established CRISPR/Cas9-mediated somatic gene disruption, allowing for in vivo deletion of candidate tumor suppressor genes. We demonstrate the utility of this approach by somatic disruption of the Ptch1 gene in the mouse cerebellum, leading to the formation of medulloblastoma faithfully resembling the SHH-driven subgroup of the disease. This in vivo method for validation of candidate tumor suppressor genes provides a fast and convenient system for the generation of faithful animal models of human cancer.

2014-12-31 | GSE58629 | GEO

A commonly inactivated tumor suppressor silences endogenous retroelements in somatic cells

Project description:A commonly inactivated tumor suppressor silences endogenous retroelements in somatic cells

| PRJNA338982 | ENA

Mus musculus

Project description:Somatic CRISPR/Cas9-mediated tumor suppressor disruption enables versatile murine cancer modeling

| PRJNA253040 | ENA

Somatic CRISPR/Cas9-mediated tumour suppressor disruption enables versatile brain tumour modelling.

Project description:In vivo functional investigation of oncogenes using somatic gene transfer has been successfully exploited to validate their role in tumorigenesis. For tumour suppressor genes this has proven more challenging due to technical aspects. To provide a flexible and effective method for investigating somatic loss-of-function alterations and their influence on tumorigenesis, we have established CRISPR/Cas9-mediated somatic gene disruption, allowing for in vivo targeting of TSGs. Here we demonstrate the utility of this approach by deleting single (Ptch1) or multiple genes (Trp53, Pten, Nf1) in the mouse brain, resulting in the development of medulloblastoma and glioblastoma, respectively. Using whole-genome sequencing (WGS) we characterized the medulloblastoma-driving Ptch1 deletions in detail and show that no off-targets were detected in these tumours. This method provides a fast and convenient system for validating the emerging wealth of novel candidate tumour suppressor genes and the generation of faithful animal models of human cancer.

| S-EPMC4467376 | biostudies-literature

The tumor suppressor kinase DAPK3 drives tumor-intrinsic immunity through the STING-IFNb pathway Phospho

Project description:Phosphoproteomics show that the tumor suppressor kinase DAPK3 drives tumor-intrinsic immunity through the STING-IFNb pathway

2021-01-15 | MSV000086706 | MassIVE

The tumor suppressor kinase DAPK3 drives tumor-intrinsic immunity through the STING-IFNb pathway Proteome

Project description:Proteome analysis reveals that the tumor suppressor kinase DAPK3 drives tumor-intrinsic immunity through the STING-IFNb pathway Proteome

2021-01-15 | MSV000086708 | MassIVE

Genetic disruption of Ctcf destabilizes DNA methylation

Project description:Ctcf heterozygous knockout mice are susceptible to neoplasia in a broad range of tissues, including lymphoma, endometrial cancer, and non-small cell lung cancer. Retention of the wild type Ctcf allele in these tumors establishes CTCF as a haploinsufficient tumor suppressor gene. Both human tumors and normal murine tissues with CTCF disruption are characterized by genome-wide differences in DNA methylation relative to CTCF wild type tissues, indicating even modest disruption of CTCF broadly destabilizes DNA methylation in vivo. This cross species functional analysis identifies CTCF as a commonly mutated tumor suppressor gene and establishes a central role for DNA methylation stability in tumor suppression. RRBS sequencing of transgenic Ctcf heterozygous mice and wild-type litter mate whole lung tissue.

2014-07-30 | E-GEOD-48975 | biostudies-arrayexpress

Leucyl-tRNA synthetase is a tumor suppressor in breast cancer and enables tumor suppressive translation

Project description:In this study, we identify leucyl-tRNA synthetase (LARS) as a breast tumor suppressor. To identify the mechanism underlying LARS-mediated breast tumor suppression, we conducted TMT-proteomics in PyMT mouse tumors with monoallelic genetic deletion of LARS in the mammary tumor compartment. The analyses implicate LARS as a regulator of leucine-rich protein translation resulting in downregulation of candidate leucine-rich tumor suppressor genes.

2022-01-10 | PXD026609 | Pride

Tumor suppressor p53 employs RFX7 and ANKRA2

Project description:Tumor suppressor p53 employs RFX7 and ANKRA2

| PRJNA680800 | ENA

RIPK3 is a tumor suppressor in mesothelioma

Project description:RIPK3 is a tumor suppressor in mesothelioma

| PRJNA666445 | ENA