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Radiation combined with KRAS-MEK inhibitors enhances anticancer immunity in KRAS-mutated tumor models [LLC RNA-seq]

ABSTRACT: KRAS mutation is a common driver in solid tumors, and KRAS-mutated tumors are relatively resistant to radiotherapy. Therefore, we investigated the combined effect of radiation and KRAS-MEK inhibitors (AMG510 and trametinib) in KRAS-mutated tumors.

ORGANISM(S): Mus musculus

PROVIDER: GSE209766 | GEO | 2022/10/01

REPOSITORIES: GEO

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Radiation combined with KRAS-MEK inhibitors enhances anticancer immunity in KRAS-mutated tumor models [CT26 RNA-seq]

Project description:KRAS mutation is a common driver in solid tumors, and KRAS-mutated tumors are relatively resistant to radiotherapy. Therefore, we investigated the combined effect of radiation and KRAS-MEK inhibitors (AMG510 and trametinib) in KRAS-mutated tumors.

2022-10-01 | GSE209765 | GEO

The expression profiles of AMG510-resistant cancer cells

Project description:AMG510 is a covalent inhibitor of G12C mutated KRAS. To identify the mechanism of resistance to AMG510, we treated MIA-PaCa2 cells with increasing dose of AMG510 for 2 months and established two population of cells that are resistant to 5 uM AMG510. RNA sequencing was used to extermine the expression profile.

2021-06-19 | GSE178479 | GEO

Differentially expressed genes in iKRAS tumor treated with Trametinib or Kras extinction

Project description:To identify the differentially expressed gene in ikras tumors treated with Trametinib or Kras extinction.

2021-06-07 | GSE176241 | GEO

Transcriptome Signature Post Reovirus Treatment In KRAS Mutated Colorectal Cancer

Project description:Reovirus propagates with high efficiency in KRAS mutated colorectal cancer (CRC). About 45-50% of CRC patients possess KRAS mutation. Oncolytic reovirus treatment in combination with chemotherapy was tested in patient samples possessing KRAS mutated metastatic CRC. This is the raw data from the peripheral mononuclear cell (PBMC) samples at 4 timepoints (pre treatment, 48 hours, day 8, and day 15).

2021-05-01 | GSE173636 | GEO

BI-3406, a potent and selective SOS1::KRAS interaction inhibitor, is effective in KRAS-driven cancers through combined MEK inhibition

Project description:KRAS is the most frequently mutated driver of pancreatic, colorectal, and non-small cell lung cancers. Direct KRAS blockade has proven challenging and inhibition of a key downstream effector pathway, the RAF-MEK-ERK cascade, has shown limited success due to activation of feedback networks that keep the pathway in check. We hypothesized that inhibiting SOS1, a KRAS activator and important feedback node, represents an effective approach to treat KRAS-driven cancers. We report the discovery of a highly potent, selective and orally bioavailable small-molecule SOS1 inhibitor, BI-3406, that binds to the catalytic domain of SOS1 thereby preventing the interaction with KRAS. BI-3406 reduces formation of GTP-loaded RAS and limits cellular proliferation of a broad range of KRAS-driven cancers. Importantly, BI-3406 attenuates feedback reactivation induced by MEK inhibitors and thereby enhances sensitivity of KRAS-dependent cancers to MEK inhibition. Combined SOS1 and MEK inhibition represents a novel and effective therapeutic concept to address KRAS-driven tumors.

2020-08-20 | GSE128385 | GEO

Radiation combined with KRAS-MEK inhibitors enhances anticancer immunity in KRAS-mutated tumor models

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

2022-10-01 | GSE209767 | GEO

Proteomics of KRAS mutated and non-transformed pancreas cells treated with ethanol

Project description:The goal for this study was to determine the effects of ethanol on pancreas cells and examine how ethanol influences protein expression in non-transformed and mutant KRAS cells. We performed TMT-labeled proteomics of non-transformed (hTERT-HPNE E6/E7) and KRAS mutated (hTERT-HPNE E6/E7/K-RasG12D) human pancreas cell lines following 6 months of 100 mM ethanol treatment.

2022-05-19 | PXD030180 | Pride

Epithelial-to-mesenchymal transition defines feedback activation of receptor tyrosine kinase signaling induced by MEK inhibition in KRAS mutant lung cancer

Project description:To determine the difference of gene expression profile in epithelial and mesenchymal KRAS mutant lung cancers, epithelial NCI-H358 cells were treated with TGFβ1 (4 ng/mL) or PBS for 14 days in order to induce epithelial to mesenchymal transition (EMT). Gene expression was determined in NCI-H358 cells before and after EMT induction. In addition, in order to investigate the effect of a MEK inhibitor trametinib on gene expression, mesenchymal NCI-H1792 cells were treated with 50 nM trametinib for 48 hours. Gene expression of H1792 cells for pre- and post-trametinib treatement was determined.

2017-03-15 | GSE79235 | GEO

The RALA pathway can maintain the proliferation of KRAS- and BRAF-mutated cancer cells

Project description:By silencing of RALA, a downstream member of the RAS signal transduction pathway, we aimed to determine whether genes downstream of a mutated KRAS (codon 12 or 13) or a mutated BRAF can have significant functions in colorectal cancer carcinogenesis.

2015-06-20 | GSE39857 | GEO

Targeting KRAS mutant cancers with a covalent G12C-specific inhibitor

Project description:We report RNAseq gene expression data following ARS-1620 treatment and shKRAS expressing cells (NCI-H358). We also compare gene expression changes following treatment with ARS-1620 or trametinib in NCI-H358, LU65 (KRAS-G12C+), and A549 (KRAS-G12S+) cells. Additionally we report a time course (4, 24, 48hr) of ARS-1620 and trametinib treated NCI-H358 cells.

2018-01-24 | GSE103021 | GEO

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