Oncostatin-M and OSM-Receptor Feed-Forward Activation of MAPK Induces Separable Stem-Like and Mesenchymal Programs

Using a panel of pancreatic ductal adenocarcinoma cells driven through epithelial-mesenchymal transition by Oncostatin-M (OSM) or the transcription factors ZEB1 or SNAI1, scientists found that OSM uniquely induces tumor-initiation and gemcitabine resistance independently of its ability to induce a CD44HI/mesenchymal phenotype.