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Modeling melanoma resistance in a genetically engineered mouse model

ABSTRACT: Modeling melanoma resistance in a genetically engineered mouse model

PROVIDER: PRJNA650202 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12365977.fastq.gz	Fastqsanger.gz
	SRR12365978.fastq.gz	Fastqsanger.gz
	SRR12365979.fastq.gz	Fastqsanger.gz
	SRR12365980.fastq.gz	Fastqsanger.gz
	SRR12365981.fastq.gz	Fastqsanger.gz

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Modeling melanoma resistance in a genetically engineered mouse model

Project description:Melanoma is the deadliest type of skin cancer and its incidence is steadily increasing. Targeting melanoma cells posseses significant challenges due to primary or acquired therapy resistance in the majority of patients. Here, we describe the generation of an in vivo mouse model mimicking the key steps in melanoma initiation, progression and resistance acquisition. The well-characterized Tyr::CreERT2 BrafV600E Ptenfl/fl mouse model was used to induce melanoma initiation and subsequently therapy resistance to a combination of BRAF (PLX4720) and MEK (PD0325901) inhibitors. Our data reveal that all of the Tyr::CreERT2 BrafV600E Ptenfl/fl mice subjected to PLX4720+PD0325901 treatment ultimately developed resistance to these inhibitors. Introduction of genetic labelling by crossing Tyr::CreERT2 BrafV600E Ptenfl/fl mice with the TdTomato reporter allele allowed us not only to observe brain metastasis, which are rarely seen in this mouse model, but also to isolate metastatic melanoma cells using flow cytometry. The comparison of the expression profile of metastatic cells before and after resistance acquisition revealed a number of pathways significantly altered in resistant cells. Here, we describe and characterize a suitable mouse model to explore the molecular and cellular mechanisms of multiple stages of drug resistance in melanoma development. Finally, this experimental model might provide further understanding of the interplay between the immune system and melanoma cells.

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