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Misia Landau, An Interview with Ronald DePinho, Clinical Chemistry, Volume 59, Issue 1, 1 January 2013, Pages 11–17, https://doi.org/10.1373/clinchem.2012.184911
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In the mid 1980s, Ronald DePinho made a career-defining decision. Convinced that most cancers arise through a host of genetic and biological changes, rather than by single mutations as was widely believed, he vowed to tackle cancer in its complexity or not at all. Believing, too, that the best way to get at cancer was to study it in a living animal, he set out to learn the new and largely untried techniques of genetic engineering and would use them to create an illuminating series of transgenic mouse models. Knocking out genes individually and in combination, DePinho and colleagues showed how specific cancer-causing proteins—such as mutant versions of the famous tumor suppressor p53—actually work. In the mid 1990s, he turned his attention to telomeres, the dense nubs of DNA on both ends of chromosomes that unravel with each cell division. Many thought that cancer cells must have an abundance of the telomere-making enzyme, telomerase. In a series of elegant experiments, DePinho and colleagues showed the opposite—that mice lacking telomerase were actually highly susceptible to cancer. Over the past 10 years, he has continued his research into the link between telomeres, cancer, and aging—work that came to widespread attention in 2010, when he and colleagues reported that by introducing telomerase they could reverse the signs of aging in mice that previously lacked the enzyme. In the past decade, he has taken a decidedly translational turn, founding the Belfer Institute for Applied Cancer Science at the Dana Farber Cancer Institute in Boston, as well as several private companies. Last year, DePinho was chosen from a field of over 70 candidates to become president of the MD Anderson Cancer Center in Houston, Texas, where he and colleagues recently launched the Institute for Applied Cancer Science. He spoke with me from his office.
