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

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

PROVIDER: PRJNA1255652 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR33319741_1.fastq.gz	Fastqsanger.gz
	SRR33319741_2.fastq.gz	Fastqsanger.gz
	SRR33319742_1.fastq.gz	Fastqsanger.gz
	SRR33319742_2.fastq.gz	Fastqsanger.gz
	SRR33319743_1.fastq.gz	Fastqsanger.gz

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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.

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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.

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