Peering into the early stages of cancer is tricky business. Oxidative stress, proliferation signals, and loss of suppressive signals from the microenvironment have all been fingered as initiating elements in the process. As DNA damage is often seen in full-blown tumors, its role has been considered, but whether it is cause or consequence of ramped-up cellular proliferation had been unclear.
In 2005, teams led by Thanos Halazonetis, now at the University of Geneva, and Jiri Bartek at the Institute of Cancer Biology in Copenhagen revealed evidence that cellular responses to DNA damage, specifically to double-strand breaks, are activated early in precancerous lesions.
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