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.
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.
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.
Pancreatic cancer, EMT, Genomic instability, Tumor evolution, Metastasis
Knockin mouse model, VimFLEX system, Exon 2-4 targeted integration, FlpO recombinase, eGFP reporter, HSV-TK for lineage ablation
From model design to experimental results
Tailor-made solutions adapted to scientific questions
Comprehensive dataset package
Generated with biopharma partners and in-house
Scientific follow-up and advice along the project
Collaborative approach for problem solving and development of innovative models
Breeding facilities in US and Europe
Certified health status from professional breeders
