Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Oncogenic KRAS(G12V) and BRAF(V600E) in intestinal organoids

ABSTRACT: Goals of the study was to compare transcripional and phenotypic response of mouse intestinal organoid cultures to the KRAS(G12V) or BRAF(V600E)oncogenes.

ORGANISM(S): Mus musculus

PROVIDER: GSE115234 | GEO | 2018/06/02

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Oncogenic KRAS(G12V) and BRAF(V600E) in intestinal organoids

Project description:Oncogenic KRAS(G12V) and BRAF(V600E) in intestinal organoids

| PRJNA474218 | ENA

Transcription profiling of human lung epithelial cells ollowing oncogenic KRAS expression and TBK1 suppression or infection with oncogenic KRAS (G12V) - SuperSeries

Project description:The proto-oncogene KRAS is mutated in a wide array of human cancers, most of which are aggressive and respond poorly to standard therapies. Although the identification of specific oncogenes has led to the development of clinically effective, molecularly targeted therapies in some cases, KRAS has remained refractory to this approach. An alternative strategy for targeting KRAS is to identify gene products that, when suppressed or inhibited, result in cell death only in the presence of an oncogenic allele. Here we have used systematic RNA interference (RNAi) to detect synthetic lethal partners of oncogenic KRAS and found that the non-canonical IkB kinase, TBK1, was selectively essential in cells that harbor mutant KRAS. Suppression of TBK1 induced apoptosis specifically in human cancer cell lines that depend on oncogenic KRAS expression. In these cells, TBK1 activated NF- B anti-apoptotic signals involving cREL and BCL-XL that were essential for survival, providing mechanistic insights into this synthetic lethal interaction. These observations identify TBK1 as a potential therapeutic target in KRAS mutant tumors and establish a general approach for the rational identification of co-dependent pathways in cancer. This SuperSeries is composed of the following subset Series:; GSE17643: Profiling of immortalized human lung epithelial cells following oncogenic KRAS expression and TBK1 suppression; GSE17671: Profiling of immortalized human lung epithelial cells following infection with oncogenic KRAS (G12V) Experiment Overall Design: Refer to individual Series

2009-10-31 | E-GEOD-17672 | biostudies-arrayexpress

Gene expression changes induced by transgenic expression of CCDC6-RET or BRAF(V600E) oncogenes in zebrafish thyroid tumors [Zebrafish RET vs BRAF adult tumors]

Project description:We used RNAseq to examine gene expression changes in thyroid tumors arising in transgenic zebrafish engineered to expression human CCDC6-RET or BRAF(V600E) oncogenes

2022-03-23 | GSE199023 | GEO

Oncogenic mutation BRAF V600E changes phenotypic behavior of THLE-2 liver cells through alteration of gene expression

Project description:The accumulation of mutations in cancer driver genes such as tumor suppressors or pro-to-oncogenes affects cellular homeostasis. Disturbances in the mechanism controlling prolifera-tion causes significant augmentation of cell growth and division due to the loss of sensitivity to the regulatory signals. Nowadays, an increasing number of cases of liver cancer are observed worldwide. Data provided by the International Cancer Genome Consortium (ICGC) have indi-cated many alterations within gene sequences, whose roles in tumor development are not well understood. A comprehensive analysis of liver cancer (hepatocellular carcinoma-virus associated) samples has identified new and rare mutations in B-Raf proto-oncogene (BRAF) in Japanese HCC patients, as well as BRAF V600E mutations in French HCC patients. However, their function on liver cancer has never been investigated. Here, using tests for functional analysis and next gen-eration sequencing we demonstrate the tumorigenic effect of BRAF V600E on hepatocytes (THLE-2 cell line). Moreover, we identified genes such as BMP6, CXCL11, IL1B, TBX21, RSAD2, MMP10, SERPIND1, which are possibly regulated by BRAF V600E-mediated mitogen-activated protein kinases/extracellular signal-regulated kinases (MAPK/ERK) signaling pathway. Through several functional assays, we demonstrated that BRAF L537M, D594A, and E648G mutations by its own are not pathogenic in liver cancer. The investigation of genome mutations and the de-termination of their impact on cellular processes and functions are crucial to unraveling the mo-lecular mechanisms of liver cancer development.

2022-01-28 | GSE194425 | GEO

KRAS mutation (G12V) expression by pBABE-Puro vector in NCI-H1703 cells

Project description:The goal of this study was to determine genes affected by expressing KRAS mutation (G12V) in NCI-H1703 cells This data was used in Meng Wang et. al. Cancer Research 2016 to determine the alterations of gene expression profiling associated with expression of KRAS mutation (G12V). The experiment uses a pBABE-Puro vector encoding KRAS G12V and a corresponding empty vector control.

2016-03-23 | E-GEOD-79486 | biostudies-arrayexpress

Murine lung tumors- HER2(V659E) and KRAS(G12V) vs normal lung

Project description:Transcriptiional profling of 13 normal lung samples, 18 lung KRAS(G12V) tumor samples, and 18 lung HER2(V659E) tumor samples 13 normal lung samples, 18 lung KRAS(G12V) tumor samples, and 18 lung HER2(V659E) tumor samples hybridized against Stratagene universal mouse reference RNA with dye swap

2009-11-30 | E-GEOD-18784 | biostudies-arrayexpress

Transcriptional Response to transgenic BRAF(V600E) in the intestinal epithelium

Project description:BRAF(V600E) is a frequent mutation in colon cancer. We have analysed transcriptional effects of BRAF(V600E) in the intestinal epithelium of transgenic mice that harbour an inducible BRAF(V600E) transgene. Mice used in this experiment were compound transgenic for a stem-cell specific Lgr5-EGFP Reporter and either an inducible TdTomato-2A-BRAF(V600E) transgene or an inducibe TdTomato-luciferase transgene. Transgenes were induced by doxycycline (4mg/ml) treatment provided in a 1% sucrose solution in the drinking water of transgenic mice for 24h. Intestinal crypts were isolated by filtering (70um) following a PBS/EDTA incubation step. Single cell suspensions were made by digestion of crypts in 500ug/ml trypsine and 0.8u/ml DNAseI for approx. 20min at RT. Cell populations for profiling were isolated by FACS, using an Aria SOPR (BD), equipped with a 70um nozzle.

2013-12-31 | E-GEOD-50678 | biostudies-arrayexpress

3' RNAseq of EGFR mutant lung cancer cell line overexpressing BRAF V600E treated with inhibitors

Project description:In the human EGFR mutant adenocarcinoma cell line PC9 pBabe empty vector (EV) or BRAF V600E were overexpressed. RNA was extracted from EV, BRAF V600E overexpressing or osimertinib-resistant BRAF V600E expressing cells after 48h treatment with osimertinib, trametinib, a combination of both or vehicle controls. RNA was subjected to 3' UTR RNA sequencing.

2021-10-20 | E-MTAB-11004 | biostudies-arrayexpress

KRAS mutation (G12V) expression by pBABE-Puro vector in NCI-H1703 cells

2016-03-23 | GSE79486 | GEO

KRAS G12V digestion by 20S proteasome

Project description:KRAS is a well known tumor associated antigen. It’s a GTPase that functions as molecular switch in regulatory pathways responsible for proliferation and survival. It’s frequently mutated in a variety of cancers. One of the possible driver mutations is G12V substitution, which impairs KRAS GTPase activity and renders the mutants persistently in the GTP-bound active form, thereby promoting tumorigenesis and tumor malignancy. Its high frequency in cancers makes KRAS an attractive target for immunotherapy. We performed in vitro digestions of synthetic polypeptide corresponding to KRAS2-35 carrying the mutation with purified 20S proteasome. Samples were measured by LC-MS/MS.

2019-10-24 | PXD015580 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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