University of Michigan PS-OP
Emerging evidence suggests that the physical environment of tumors, including mechanical stress and physico-chemical properties of extracellular matrix, combines with genetics and cell signaling to control plasticity of cancer stem cells during metastasis, the cause of death for > 90% of patients with cancer. Metastasis encompasses processes associated with mesenchymal (invasion) and epithelial (proliferation) phenotypes. Epithelial to mesenchymal (EMT) and mesenchymal to epithelial (MET) transitions define subsets of cancer stem cells, which are implicated as critical drivers of metastasis. In particular, circulating tumor cells (CTCs) and other disseminated tumor cells commonly exhibit both epithelial and mesenchymal features, suggesting that cancer cells transition between these states. Studies of plasticity in cancer stem cells have focused predominantly on primary tumors, in part due to technological challenges of analyzing cell phenotypes and dynamics in other anatomic sites.