If the scientist’s job is to ponder the stars, the banker’s is to funnel his vision into stellar panels. For while scientific theory can be enthralling, it’s in danger of racking up lost gigabytes and circuitry dust. But when a smart businessman and a top scientist get together, not only can the partnership lead to pragmatic accomplishments, it can actually change the course of scientific inquiry.
Such has been the case at Harvard. The study of evolution is always moving, but nowhere has it been livelier than in Brattle Square, where, ten years ago, a financier named Jeffrey Epstein set up the Program for Evolutionary Dynamics with a $30 million gift to the university, $6.5 million of which was a current-use gift to the PED. His mission was not to coddle neo-Darwinian theorists (because, honestly, couldn’t $30 million be used to vaccinate the entire country of Zaïre?) but to embolden a pragmatic use for the study of natural selection.
It was in August 2003, with the cooperation of Lawrence Summers, then president of Harvard, that the Program for Evolutionary Dynamics set up for business, and, under the direction of Martin Nowak, a professor of mathematics and biology, it revolutionized the way in which evolution is studied and utilized. PED became one of the first programs to give a high priority to the use of mathematics in studying the evolution of microbiology. It also became one of the first departments to develop a mathematical model of how human cancer cells evolve, as well as infectious bacteria and viruses such as HIV. The program’s models have led to key discoveries toward combatting diseases of all kinds and have encouraged researchers around the world to make new discoveries of their own.
It all started in early 2000 when Epstein, a New York hedge-fund manager with a passion for cutting-edge science, invited Nowak to organize a conference on the evolution of language. Nowak was then head of the Program in Theoretical Biology at the Institute for Advanced Study at Princeton and had already published a substantial amount of work on the mathematics of the HIV virus, infectious bacteria, and cancer cells. Before going to Princeton, Nowak had been the head of the mathematical-biology group at Oxford University. His work was not just theoretical but keenly practical.
By 2003, Epstein already had a substantial track record in science philanthropy. He had supported the research of many prominent scientists, including Stephen Hawking, Marvin Minsky, Eric Lander, George Church, and Nobel laureate physicists Gerard ’t Hooft, David Gross, and Frank Wilczek. He was also a member of the New York Academy of Science, a member of Rockefeller University’s board, and actively involved in the Santa Fe Institute, the Quantum Gravity Program at the University of Pennsylvania, and the Mind, Brain & Behavior Advisory Committee at Harvard. Epstein himself was not a scientist per se. He had studied physics at Cooper Union in New York and mathematics at the Courant Institute in New York, leaving both without a degree, and moved on to teaching calculus and physics at the Dalton School in Manhattan. He was then scooped up into options trading on Wall Street and applied his acumen and mathematical wit to the markets.
But Epstein’s heart remained in the pure sciences. He was fascinated by fundamental questions on the one hand and, on the other, eager to apply scientific theory to the real world. It was this combination that drew him to Nowak. For not only was Epstein eager to probe a brilliant mind about the origins of life, but, with his connections at Harvard, he was able to provide Nowak a powerful platform to put groundbreaking medical research into immediate practice.
One of the major diseases that the program studies is human cancer. In 2012, Nowak and two postdoctoral students, Benjamin Allen and Ivana Bozic, developed the first mathematical model of how human colon-cancer cells evolve and specifically how they become immune to inhibitor-drug therapy. Their research was conducted at the request of the Pathology and Oncology Department at Johns Hopkins University. The department was trying to understand how the KRAS gene in colon-cancer cells becomes activated after inhibitor-drug therapy, making the cells resistant to treatment.
By developing a mathematical model of the growth of colon-cancer cells, Nowak and his team showed that the KRAS gene is not actually activated or “switched on” by inhibitor therapy; rather, a small percentage of colon-cancer cells with an already activated KRAS gene are immune from the start and come to predominate as the other cancer cells are destroyed by the inhibitor drug. The discovery was critical in changing the approach to inhibitor-drug therapy. Instead of applying drugs in sequence to fight secondary and tertiary resistance, the researchers at Johns Hopkins are now exploring the effects of using a cocktail of inhibitor drugs to capture all colon-cancer cell types: those with the activated KRAS gene and those without. The same tailored approach is underway for other cancers.