Tumour initiation results from a mutation acquired, for example, in a cell proliferation-regulating oncogene, for example the MAP kinase BRAF in melanoma, thyroid, ovarian and colorectal cancer. As a protective response to this initial proliferative stimulus, tissues induce a growth-arrest program termed oncogene-induced senescence (OIS). It remains largely unknown by which mechanisms the initiated cells eventually escape from the dormant OIS state.
