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RNA-seq analysis of bulk Human and single-cell Musashi2-CreER-MycT58A R26-LSL-tdTomato Mouse Pancreas ASCP, PDAC, and ACC Tumors

ABSTRACT: RNA-seq analysis of bulk Human and single-cell Musashi2-CreER-MycT58A R26-LSL-tdTomato Mouse Pancreas ASCP, PDAC, and ACC Tumors

PROVIDER: PRJNA1006761 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25694438_1.fastq.gz	Fastqsanger.gz
	SRR25694438_2.fastq.gz	Fastqsanger.gz
	SRR25694439_1.fastq.gz	Fastqsanger.gz
	SRR25694439_2.fastq.gz	Fastqsanger.gz
	SRR25694440_1.fastq.gz	Fastqsanger.gz

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Project description:Identifying the cells from which cancers arise, and the paths they take towards malignancy is critical for understanding the molecular basis of tumor initiation and progression. To determine whether stem and progenitor cells can serve as cells of origin for cancer, we created a new Msi2-CreERT2 knock-in strain. When crossed to a conditional CAG-LSL-MycT58A model, Msi2-CreERT2 mice developed multiple pancreatic cancer subtypes: pancreatic ductal adenocarcinoma (PDAC), adenosquamous carcinoma of the pancreas (ASCP), acinar cell carcinoma (ACC), and rare anaplastic tumors. Combining single-cell genomics with computational analysis of developmental states and lineage trajectories, we demonstrate that oncogenic MYC preferentially triggers the transformation of the most immature subset of Msi2+ cells, leading to the rise of a common pool of pre-cancer cells with multi-lineage properties. These pre-cancer cells subsequently diverge to distinct pancreatic cancer subtypes by activation of distinct transcriptional programs and large-scale genomic changes. Importantly, the enforced expression of specific molecular signals can redirect cells toward specific subtypes. This study shows that multiple pancreatic cancer subtypes can arise from a common pool of Msi2+ cells and provides a powerful framework to understand and control the programs that shape divergent fates in pancreatic cancer.

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