BLOOMSBURY SIGMA, FEBRUARY 2015In 2002, Larry Donehower of Baylor College of Medicine in Houston, Texas, was creating a mouse model to explore the workings of the tumor suppressor gene p53 when he made a surprisingly fruitful mistake. Donehower had used an unfamiliar technique to create a mouse with p53 knocked out, and so, instead, he ended up with mice in which the gene was not only still present, but hyperactive. Predictably, his super-p53 critters proved highly resistant to developing tumors. But what no one expected to see was that they aged exceptionally fast: within months their fur was bedraggled and gray, their backs hunched, and they died prematurely, losing about 30 percent of their normal life span.
That aging and cancer were related was common knowledge, since the risk of cancer increases with age. But few suspected they might be two sides of the same coin, sharing a mechanism through which the scales could be tipped either way.
As I researched and wrote p53: The Gene That Cracked the Cancer Code, I became intrigued by how often apparent experimental failures have provided vital clues to unraveling the mysteries of this particular gene. Even the discovery of p53, in 1979, was arguably the result of failure. By coincidence, four different labs, working independently and unaware of each other’s quests, discovered p53 simultaneously. Three were working with the oncogenic monkey virus SV40, trying to isolate the specific viral gene and its protein product responsible ...
