Abstract
Cellular plasticity endows cancer cells with capacity towards a phenotypic state. Except from the genetic origin of cellular plasticity, cancer cells can transit to reversible phenotypic states as a result of microenvironmental cues and are often driven by stochastic epigenetic and/or transcriptional fluctuations. Melanoma is a prime example of heterogeneous and plastic tumors where the origin and magnitude of cell state diversity remains poorly understood. Combining lineage tracing, 3D imaging and quantitative mathematical modelling in a clinically-relevant mouse model of melanoma, we demonstrated that tumors follow a hierarchical model of growth supported by a population of Melanoma Stem-like Cells (MSCs) that exhibit a transcriptomic signature of pre-migratory neural crest cells established transiently during embryonic development.
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