Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Kinome-wide shRNA screen for synthetic lethality in patient-derived FANCA-deficient fibroblasts.

ABSTRACT: Kinome-wide shRNA screen for synthetic lethality in patient-derived FANCA-deficient fibroblasts.

PROVIDER: PRJEB44964 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	ERR5925040.fastq.gz	Fastqsanger.gz
	ERR5925050.fastq.gz	Fastqsanger.gz
	ERR5925041.fastq.gz	Fastqsanger.gz
	ERR5925051.fastq.gz	Fastqsanger.gz
	ERR5925042.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 15

Similar Datasets

Kinome-wide shRNA screen for synthetic lethality in patient-derived FANCA-deficient fibroblasts.

Project description:The purpose of this screen was to identify synthetic lethal targets in FANCA-deficient cells.

2021-05-24 | E-MTAB-9802 | biostudies-arrayexpress

CRISPR-Cas9 RBM10 synthetic lethality screen

Project description:CRISPR-Cas9 RBM10 synthetic lethality screen

| PRJEB60386 | ENA

Synthetic lethal siRNA screen for TN-IBC cell line SUM149PT using kinome library with EPA treatment

Project description:Synthetic lethal siRNA screen using a kinome library containing 939 druggable genes in the TN-IBC cell line SUM149PT, in combination with EPA treatment.

2019-01-31 | GSE102057 | GEO

Kinome and Rho-GTPase Synthetic Lethal shRNA Library Screen in paired NF1-/- and GAP-Related Domain Restored Schwann Cells

Project description:To identify possible novel targets for the treatment of plexiform neurofibroma formation through a synthetic lethal shRNA library screen in the tumorigenic cell of origin, Schwann cells.

2019-11-30 | E-MTAB-8398 | biostudies-arrayexpress

shRNA cassette sequencing from disomic and trisomic fibroblasts cultured in the presence of shRNA kinome library for 14 days

Project description:Kinome-wide shRNA screen to identify kinases differentially required for survival of cells disomic and trisomic for chromosome 21

2016-07-29 | GSE79840 | GEO

ARID1A KLF5 synthetic lethality CRISPR screen in U2OS cells

Project description:ARID1A KLF5 synthetic lethality CRISPR screen in U2OS cells

| PRJEB75512 | ENA

Profound synthetic lethality between SMARCAL1 and FANCM (CRISPR screen)

Project description:Profound synthetic lethality between SMARCAL1 and FANCM (CRISPR screen)

| PRJNA1157381 | ENA

shRNA cassette sequencing from disomic and trisomic fibroblasts cultured in the presence of shRNA kinome library for 14 days

Project description:Kinome-wide shRNA screen to identify kinases differentially required for survival of cells disomic and trisomic for chromosome 21 Cells were transduced in triplicate and propagated for 14 days to allow for enrichement or depletion of shRNAs from the population

2016-07-29 | E-GEOD-79840 | biostudies-arrayexpress

Kinome and Rho-GTPase Synthetic Lethal shRNA Library Screen in paired NF1-/- and GAP-Related Domain Restored Schwann Cells

Project description:Kinome and Rho-GTPase Synthetic Lethal shRNA Library Screen in paired NF1-/- and GAP-Related Domain Restored Schwann Cells

| PRJEB34683 | ENA

Identifying and Exploiting Combinatorial Synthetic Lethality by Characterizing Adaptive Kinome Rewiring of EGFRvIII-driven Glioblastoma

Project description:GBM is an aggressive primary malignant brain tumor that has a poor prognosis. Molecular characterization of GBM has shown that EGFR mutations are present in over 50% of tumors. However, EGFR inhibitors have not shown clinical efficacy in contrast to other EGFR-driven neoplasms due to the unique EGFR biology found in GBM. We believe that upfront combinatorial therapy with EGFR inhibitors can overcome these challenges. To identify combinatorial drug targets, we temporally characterized drug induced EGFRvIII kinome rewiring in a cell line with an isogenic genetically engineered GBM EGFRvIII kinome. Kinomic characterization show that kinome rewiring has both shared and unique kinases after acquired resistance develops despite a common genetic origin. Additionally, we noted that the kinases altered in the acute setting are distinct from those in acquired resistance. By identifying these differential temporal kinomic vulnerabilities throughout the drug response process, we generated a kinase signature associated with inhibition of EGFR. Further molecular interrogation of these signature genes reveals that drug treatment induces an unexpected increase in Cdk6 protein but not mRNA despite a decrease in proliferation measured by both live cell counts and transcriptomics. Survival experiments with two cohorts of orthotopic allografts show that upfront combination inhibition of Cdk6, with abemaciclib, and EGFR, with neratinib, significantly prolonged median survival compared to neratinib alone. Our findings suggest that identifying and inhibiting targets with synthetic lethality in the upfront combinatorial setting is a viable approach for precision oncology and may help provide an avenue to overcome the resistance mechanisms that contributed to the failures of EGFR as a molecular target in GBM.

2025-06-28 | GSE296151 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data