Evolutionary fingerprints of epithelial-to-mesenchymal transition

Luigi Perelli
European Institute of Oncology (IEO)
March 5, 2025
Nature
https://pubmed.ncbi.nlm.nih.gov/40044861

This article is currently being updated. View its version on PubMed.

https://pubmed.ncbi.nlm.nih.gov/40044861

Research summary

This study investigates the role of epithelial-to-mesenchymal transition (EMT) in pancreatic cancer progression, highlighting its impact on tumor heterogeneity, clonal evolution, and metastatic dissemination.

Key outcome of the study

EMT contributes to chromosomal instability, including chromothripsis. Mesenchymal lineages exhibit increased chromatin accessibility, delayed mitosis, and catastrophic cell division. Ablation of mesenchymal lineages halts mutational processes and tumor evolution.

Model

VimFLEX(SA-H2B-eGFP-T2A-FlpO-WPRE-pA) and VimFLEX(SA-eGFP-T2A-HSV-TK-WPRE-pA) mouse models generated by genOway, targeting exons 2 to 4 of the Vim gene while minimizing regulatory element interference. These models enable lineage tracing and ablation of mesenchymal tumor cell populations.

TARGET:
Vim
Synonyms:
Vimentin

Keywords

Pancreatic cancer, EMT, Genomic instability, Tumor evolution, Metastasis

Technical specifications

Knockin mouse model, VimFLEX system, Exon 2-4 targeted integration, FlpO recombinase, eGFP reporter, HSV-TK for lineage ablation

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