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Targeted degradation of oncogenic KRAS G12V triggers antitumor immunity in lung cancer

ABSTRACT: Targeted degradation of oncogenic KRAS G12V triggers antitumor immunity in lung cancer

PROVIDER: PRJNA981494 | ENA |

REPOSITORIES: ENA

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Targeted degradation of oncogenic KRAS G12V triggers antitumor immunity in lung cancer [bulkRNA-Seq]

Project description:We performed bulk-RNA sequencing analysis from KRAS G12V mouse tumor nodules from different treatment.

2024-12-18 | GSE234470 | GEO

Targeted degradation of oncogenic KRAS G12V triggers antitumor immunity in lung cancer [scRNA-seq]

Project description:We performed single cell RNA sequencing analysis from KRAS G12V mouse tumor nodules from different treatment.

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

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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

Targeted degradation of oncogenic KRAS G12V triggers antitumor immunity in lung cancer

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

2024-12-18 | GSE234472 | GEO

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

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

2016-03-23 | GSE79486 | GEO

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

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

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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

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