Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptomic characterization of sotorasib-resistant tumors in Kras-G12C/Trp53-driven LUAD in genetically engineered mice

ABSTRACT: Transcriptomic characterization of sotorasib-resistant tumors in Kras-G12C/Trp53-driven LUAD in genetically engineered mice

PROVIDER: PRJNA842081 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR19391248.fastq.gz	Fastqsanger.gz
	SRR19391249.fastq.gz	Fastqsanger.gz
	SRR19391250.fastq.gz	Fastqsanger.gz
	SRR19391251.fastq.gz	Fastqsanger.gz
	SRR19391252.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 16

Similar Datasets

Transcriptomic characterization of sotorasib-resistant tumors in Kras-G12C/Trp53-driven LUAD in genetically engineered mice

Project description:To characterize sotorasib resistance in lung adenocarcinomas (LUAD), we generated genetically engineered mice (Kras-G12C, Trp53-KO) and compared the transcriptional profiles of untreated and sotorasib-resistant tumors

2023-03-05 | GSE204752 | GEO

Transcriptomic analysis of sotorasib-resistant patient-derived xenograft (PDX) lung tumor cells

Project description:To characterize sotorasib resistance in lung adenocarcinomas (LUAD), we implanted pieces derived from a patient-derived KRAS-G12C positive xenograft (PDX) lung tumor model in immunocompromised mice

2023-03-05 | GSE204753 | GEO

Development of acquired resistance to sotorasib in NCI-H358 cell line in vitro

Project description:NCI-H358 is a KRAS G12C-mutant non-small lung cancer cell line known to be sensitive to KRAS G12C-inhibitor sotorasib. Here, we aimed to develop sotorasib resistance in H358 and interrogate the resulting sotorasib-resistant cell line (H358-R). The H358-R cell line was created by continuous culturing of the H358 cells in sotorasib (250 nM) until cells grew readily under sotorasib pressure (approximately 2 months). We then performed RNA-seq of the resulting sotorasib-resistant cell line (H358-R) with and without sotorasib pressure, compared to the parental sensitive cell line control (H358). KRAS gene expression level was found to be increased in the sotorasib-resistant line compared with the parental cells, likely representing a mechanism of resistance. The increased KRAS expression level in the resistant cell line was maintained under sotorasib pressure.

2025-09-24 | GSE277630 | GEO

RNA-seq data for H-23 and H-358 parental and sotorasib-resistant lines

Project description:We measured gene expression using RNA-sequencing for two cell lines (H-23 and H-358) parental and their sotorasib-resistant equivalent without treatment or treated with with G12C KRAS inhibitor sotorasib (AMG510)

2023-04-26 | GSE229070 | GEO

ATAC-seq of NCI-H358 cells treated with KRAS G12C inhibitor sotorasib

Project description:ATAC-seq of sotorasib-resistant NCI-H358 cells treated with sotorasib

2025-07-15 | GSE266309 | GEO

ATAC-seq of NCI-H358 cells treated with KRAS G12C inhibitor sotorasib

Project description:ATAC-seq of NCI-H358 cells treated with KRAS G12C inhibitor sotorasib

| PRJNA1106537 | ENA

CDK12/13 inhibition in NSCLC cell lines with acquired resistance to sotorasib

Project description:The efficacy of KRAS-G12C inhibitors in lung cancer is limited by the rapid onset of acquired resistance. While divergent mechanisms of resistance across patients and preclinical models have complicated efforts to identify therapeutic strategies for sotorasib-resistant cancers, we found that sotorasib-resistant H358 and LU65 cell lines, which have distinct mechanisms of resistance and drug sensitivity profiles, both exhibited increased vulnerability to treatment with SR-4835, an inhibitor of the transcriptional kinases CDK12 and CDK13. To identify CDK12/13-dependent genes linked to the increased sensitivity we observed in sotorasib-resistant over parental cells, we treated parental and sotorasib-resistant H358 and LU65 cells with SR-4835 and performed RNA sequencing.

2025-10-07 | GSE288707 | GEO

Sotorasib Resistance in KRAS G12C-Mutant Invasive Mucinous Adenocarcinoma with Implications for VEGF-A

Project description:Invasive mucinous adenocarcinoma (IMA) is a rare subtype of lung adenocarcinoma with a poor prognosis. Compared to non-small cell lung cancer (NSCLCs), IMA more frequently harbors KRAS mutations in the order KRAS p.G12V, p.G12D, and p.G12C. This report describes a patient with KRAS p.G12C-mutant IMA treated with sotorasib. To date, no studies have investigated the therapeutic efficacy or resistance mechanisms of sotorasib in IMA. The patient was treated with carboplatin and pemetrexed, followed by sotorasib upon disease progression. While the primary lung lesions responded well, metastatic thoracic lymph node lesions continued to increase. A pathological autopsy was performed with the family’s consent to investigate potential resistance mechanisms. RNA sequencing and additional analyses revealed increased VEGF-A expression in metastatic lymph node lesions, suggesting a role in sotorasib resistance. These findings provide insights into the molecular mechanisms underlying treatment resistance in KRAS p.G12C-mutant IMA.

2025-05-02 | GSE295712 | GEO

Genetic changes of sotorasib-resistant cells

Project description:Sotorasib-resistant cells were established by exporsure of LU65 and MiaPACA-2 cells to increasing dose of sotorasib, up to 5 micromole. Exome sequencing was done to study the genetic changes.

2023-01-01 | E-MTAB-12144 | biostudies-arrayexpress

Sotorasib Resistance in KRAS G12C-Mutant Invasive Mucinous Adenocarcinoma with Implications for VEGF-A

Project description:Sotorasib Resistance in KRAS G12C-Mutant Invasive Mucinous Adenocarcinoma with Implications for VEGF-A

| PRJNA1255652 | ENA