She chopped and sliced the tumor into samples, based on a list that Steinman helped draw up beforehand. A few grams would be placed in screw-top vials filled with a preservative for their RNA. Steinman’s administrative assistant would take another piece to Boston on an afternoon train, and some would go to a former student, Kang Liu, so she could sew confetti-sized squares of the tumor into living mice. If there was any left, they would send it to a researcher in Baltimore named Elizabeth Jaffee, who had mastered the art of culturing pancreatic cancer in a dish.

The mass was big enough that Schlesinger could get through all the items on the list. In the days, weeks and months that followed, Steinman’s cancer was sent to labs in Boston and Baltimore, Toronto and Tübingen, Germany, Dallas and Durham, N.C. With help from friends and former students, he would squeeze every bit of data from his cancer that he could.

Steinman’s last experiment would be, in many ways, the culmination of a new trend in cancer research: designing custom treatments for each patient. When he got sick, Steinman knew that the five-year survival rate for his kind of tumor was, at most, 1 in 10, even at Sloan-Kettering, one of the best oncology centers in the world. Typically, patients live six months. But he also knew that his chances might not be as bad as they looked. The means and medians of his disease were drawn from populations and so did not reflect the fact that every tumor is unique. Even tumors that look the same — cancers starting from a common organ, or a common kind of cell — may behave in different ways: some shrink and some expand; some succumb to chemotherapy. Now doctors can scan each tumor for clues about its DNA and use those clues to determine its strengths and weaknesses. Steinman could have his case described right down to the letters of its genome, in hopes of figuring out which therapies might work best for him.

This “personalized” approach to treating cancer, which subdivides the classic types according to distortions in their genes, has been growing at a rapid pace. In the past few years, laboratories financed by the government have set out to build a comprehensive atlas of the cancer genome — to collect 500 tumors from each of 25 kinds of the disease and then to analyze their DNA and RNA at a cost of more than $100 million a year. The advent of inexpensive genome sequencing has produced a gold rush in the commercial sector, too, with the promise that anyone’s tumor can be sliced and processed and analyzed, until its genetic fingerprint is decoded.

“It was thought a while ago that cancer would be too complex for us to really get our hands around it,” says Raju Kucherlapati, one of the principal investigators on the Cancer Genome Atlas and a professor of genetics at Harvard Medical School. But current research showed that “the total number of major biochemical pathways that are altered is not limitless.” If that’s true, then doctors might use these genomic data to improve their patients’ odds. Instead of applying a one-size-fits-all approach to treatment, they could select a mix of therapies from a standard arsenal, choosing only those that matched the features of a patient’s tumor. “I would venture to say that within the next 10 years, we could see a very significant revolution in the way that we think about and treat cancer,” Kucherlapati says.

The genomic approach that Kucherlapati and others have advanced sees every person’s cancer as a snowflake — a crystal made from several dozen basic shapes. But this idea has lately run across a deeper layer of complexity and one that is only now being outlined in the lab. For a paper published in the spring of 2012, a group of scientists based in London looked at tiny pebbles of disease from four kidney-cancer patients. Instead of limiting their analysis to a single piece of each tumor — one piece of tissue, excised after surgery or drawn out through a needle — the researchers took malignant cells from all over the patients’ bodies. They sliced specimens from more than half a dozen spots on the primary tumor, and then more from places where the cancer had spread: in the lungs, the chest wall and the fat surrounding the kidneys. When they compared the genomes at each location, they found a whole suite of tumor types with only a distant family resemblance, as if each spot and organ had become the home for its own phylum of disease. The growths were related — they had all descended from a common ancestor — but the cancer had mutated in new directions, sprouting a canopy of branches and twigs on its evolutionary tree. Samples drawn right from a kidney — as close as possible to where the tumor started — shared only a third of their mutations with the other offshoots.

Image Ralph Steinman in 1983. He would become his most compelling experiment. Credit... Steinman: Photograph by Ingbert Grüttner/Rockefeller University. Dendritic cell: Rockefeller University Press.

A number of recent studies came to similar conclusions. Taken together, they reiterate what has long been known but not quite grasped in such detail: that even a single cancer patient carries a private ecosystem of pathology within her body, a tropical rain forest of disease. If the old chemotherapies and radioactive treatments worked like napalm to blast away the canopy, the new breed of personalized therapies target only specific plants. For some cancers, the more homogeneous ones, they do the job just fine. For others, though, the approach comes up against the relentless rules of Darwinian selection. Wipe out one subtype of a cancer — the clone that seems most aggressive, say, or the one that’s most prevalent in a biopsy — and you may have slowed the disease or thinned it out. But the cells left behind might represent a fitter strain and fill the niche.