  Tumors are defined by their intense proliferation, but sometimes cancer cells
turn senescent and stop replicating. In the stochastic cancer model in which
all cells are tumorigenic, senescence is seen as the result of random
mutations, suggesting that it could represent a barrier to tumor growth. In the
hierarchical cancer model a subset of the cells, the cancer stem cells, divide
indefinitely while other cells eventually turn senescent. Here we formulate
cancer growth in mathematical terms and obtain predictions for the evolution of
senescence. We perform experiments in human melanoma cells which are compatible
with the hierarchical model and show that senescence is a reversible process
controlled by survivin. We conclude that enhancing senescence is unlikely to
provide a useful therapeutic strategy to fight cancer, unless the cancer stem
cells are specifically targeted
