8 Oct 2010
Cavendish Laboratory of Physics, Cambridge, and
Department of Systems Biology, HMS
UV B (UVB) radiation induces mutations to the p53 tumor suppressor gene, leading to skin cancer. How do the earliest p53 mutant cells behave? Do these cells already disrupt homeostasis? In this talk I will discuss how clone size statistics from mice and humans exposed to UVB radiation discloses the growth dynamics of p53 mutant clones . The data show that p53 mutation leads to excess cell proliferation very early on; but ending UVB exposure rebalances p53 mutant behaviour. This has implications for deciding how to plan your time on the beach: ongoing low-intensity UVB radiation increases the number of precancerous cells dramatically compared with sporadic, higher-intensity exposure at the same cumulative dose. Repeating these experiments with several transgenic mice provides hints of the mechanism underlying loss of homeostasis in p53 mutant cells.
current theory lunch schedule