Recent Advances in p53 Research and Cancer Treatment

Figure 1

Vousden and Prives [2] proposed a model of the dual mechanism of p53 function in tumors. The result of p53 activation depends on multiple variables. In this model, the p53 response to low stress results in cell cycle arrest, growth inhibition, DNA repair, and so on. This response enables cells to restore the damage induced by the cellular stress. But when the cells receive high stress that cannot be restored, p53 acts as killer that can induce apoptosis or senescence, preventing proliferation of defective cells. If p53 mistakenly responds as a protector when cells receive a high stress that cannot be repaired, the cells keep the genetic damage, which can lead to or contribute to cancer progression (dotted line).