Alexandra Jilkine

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  Stochastic models of stem cell dedifferentiation in cancer
  Alexandra Jilkine
  Recent evidence suggests that, like many normal tissues, many cancers are maintained by a small population of cancer stem cells that divide indefinitely to produce more differentiated cancerous cells.

  
  Tissues, however, contain many more differentiated cells than stem cells, and mutations may cause such cells to "dedifferentiate" into a stem-like state.
  We study the effects of dedifferentiation on the time to cancer onset and found that the effect of dedifferentiation depends critically on how stem cell numbers are controlled by the body. If homeostasis is very tight (due to all divisions being asymmetric), then dedifferentiation has little effect, but if homeostatic control is looser (allowing both symmetric and asymmetric divisions), then dedifferentiation can dramatically hasten cancer onset and lead to exponential growth of the cancer stem cell population. We also consider effects of various negative feedback loops from the progenitor population on regulation of homeostasis.
  Our results suggest that dedifferentiation may be a very important factor in cancer and that more study of dedifferentiation and stem cell control is necessary to understand and prevent cancer onset.