Theory Lunch this week

October 6, 2010 § Leave a comment

How does the first cell in a tumor behave?

Friday, 8 Oct 2010, 12pm
Warren Alpert 563 – HMS

Allon Klein
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 [1]. 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.

1.    A M Klein, D E Brash, P H Jones, B D Simons, “Stochastic fate of p53-mutant epidermal progenitor cells is tilted toward proliferation by UV B during preneoplasia”, PNAS 107:270-275 2010. PubMed

Theory Lunch schedule


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