Tania Stutman's doctor was tactful but blunt: She had one year left to live. The cancer in her small bowel, he explained, was rare and untreatable. “Go home and get your affairs in order,” Stutman recalls the doctor saying. That was in 1998. But Stutman, 49 at the time, defied the odds. She survived her gastrointestinal tumor for the next three years, long enough to take part in a clinical trial of a pioneering new drug called Gleevec. Within two months, Stutman saw her tumor shrink by 50 percent. She's been taking Gleevec every day since.
See also: Major events in the history of cancer.
In this era of pink ribbons and yellow Livestrong bracelets and a proliferation of races to cure cancer, it's easy to forget that just three or four decades ago, a cancer diagnosis was likely a death sentence. In the early 1970s, the five-year survival rate for all invasive cancers was a dismal 43 percent, and the treatments — disfiguring surgery, almost unbearably toxic chemotherapy, indiscriminate radiation — were so dreadful that many patients considered them worse than the disease.
Today, the five-year survival rate for all cancers is 67 percent. Surgery, chemotherapy and radiation — still the triad of successful cancer treatment — are more precise, causing much less pain and disfigurement. But the real turning point for patients like Stutman occurred in 1971, with the signing of the National Cancer Act.
A 'scary smart' opponent
The Act provided an enormous bump in funding for the National Cancer Institute, which led to the development of dozens of federally designated cancer-research facilities nationwide. Those facilities attracted the best minds — which, in turn, launched an explosion of research into the molecular underpinnings of cancer. And that has led to novel treatments and a huge upswing in the number of cancer survivors, from just 3 million in 1971 to about 12 million in 2012.
So what makes cancer such a fierce opponent? It's smart. "Scary smart," says Richard Schilsky, M.D., section chief of hematology and oncology at University of Chicago Medicine. All cancers share the trait of pathological cell division, but beyond that, they vary as much as height and weight among the general population. Because of that, a successful treatment for, say, colon cancer won't work for lung cancer.
The reason stems from cancer's molecular origins. Cells naturally replicate, either to sustain growth or to replace cells that have died. In healthy cells, this duplication is regulated, allowing for what our bodies need and no more. In cancerous cells, mutations take place at the genetic level, prompting cells to duplicate unabated, leading either to a tumor or, in the case of blood cancers, exceedingly high white blood cell counts. Much of the cancer research over the last four decades has been in pursuit of unlocking the mystery of these mutations — what causes them and how to repair them or block their effects.
In addition to its molecular complexity, cancer presents another abstruse puzzle: heterogeneity. Most cancers have not one type of mutation but hundreds, often in many different combinations. And the same cancer can differ from patient to patient.