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Cell-state transitions and frequency-dependent interactions among subpopulations together explain the dynamics of spontaneous epithelial-mesenchymal heterogeneity in breast cancer
Abstract Individual cells in a tumour can be distributed among Epithelial (E) and Mesenchymal (M) cell-states, as characterised by the levels of canonical E and M markers. Even after E and M (E-M) subpopulations are isolated and then cultured independently, E-M heterogeneity can re-equilibrate in each population over time, sometimes …