For more than 60 years, Robert Martensen’s lung cells replicated without a hitch, regulated by specialized enzymes called kinases. Much like thermostats that adjust the temperature in a room to make sure it’s not too hot or too cold, kinases make sure that the right number of new cells are created as old ones die. But sometime in his early sixties, something changed inside Martensen. One or more of the genes coding for his kinases mutated, causing his lung cells to begin replicating out of control.
At first the clusters of rogue cells were so small that Martensen had no idea they existed. Nor was anyone looking for them inside the lean, ruddy-faced physician, who exercised most days and was an energetic presence as the chief historian at the National Institutes of Health. Then came a day in February 2011 when Martensen noticed a telltale node in his neck while taking a shower. “I felt no pain,” he recalls, “but I knew what it was. I told myself in the shower that this was cancer—and that from that moment on, my life would be different.”
Martensen initially thought it was lymphoma, cancer of the lymph glands, which has a higher survival rate than many other cancers. But after a biopsy, he was stunned to discover he had late-stage lung cancer, a disease that kills 85 percent of patients within a year. Most survive just a few months.
Once the diagnosis was made, two questions consumed the oncologists fighting to save Martensen’s life: What was the mechanism causing the mayhem in his cells? And how could they switch that mechanism off to stop the tumor growing inside him?
Despite decades of work and billions of dollars spent to combat cancer, the odds were that no one could definitively answer either question for Robert Martensen. Every person’s cancer is a bit different genetically, making it difficult to identify its exact molecular fingerprint or to target it with drugs. That lack of precision forces physicians to give nearly all cancer patients front-line treatments, including chemotherapies, that are not only toxic but also tend to have a low rate of success. If these fail, doctors are forced into a trial-and-error approach with second- and third-line therapies, hoping to get lucky.
