Epithelial-to-mesenchymal transition is dispensable for metastasis but induces chemoresistance in pancreatic cancer

By Xiaofeng Zheng, Julienne L. Carstens, Jiha Kim, Matthew Scheible, Judith Kaye, H. Sugimoto, Chia-Chin Wu, Valerie S. LeBleu, Raghu Kalluri. Nature, 2015

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The molecular mechanisms and therapeutic strategies of EMT in tumor progression and metastasis (2022, background): “Two separate studies have found that in genetically engineered mouse models of breast and pancreatic cancer, the primary and metastatic tumor cells became resistant to chemotherapeutic agents with an EMT-dependent presentation [185, 186].”
EMT, MET, plasticity and tumor metastasis (2020, background): “Furthermore, they concluded that EMT is achieved through a complex interplay between multiple EMT-TFs and that a system that deletes one factor is unlikely to capture the entire complexity [26].”
Epithelial–mesenchymal transition in tumor metastasis (2016, background): “…Pdx1-Cre) genetic engineered mouse model of pancreatic ductal adenocarcinoma and found that deletion of SNAIL1 or TWIST1 did not lead to any significant difference in metastatic potential and the number of CTCs, but rather an increased sensitivity to gemcitabine treatment (Zheng et al., 2015).”