Jun.2 – 4

Arizona State University
Tempe, AZ

Cancers are diseases of evolution. Their high mutation rates makes them hard to treat because they rapidly generate drug resistance. Infectious diseases are also a struggle between evolving pathogens and our immune systems, and the drugs that we employ. Most current drugs are designed to kill the cancer or pathogen cells. I shall describe a fundamentally different strategy: drugs that target evolvability itself. We discovered that the response of cells to external threats is controlled by distinctive molecules that can boost mutations, and hence their ability to evolve. Such ‘mutator switch’ mechanisms provide promising drug targets. Taking aim at evolutionary mechanisms in both cancers and infectious diseases might allow current drugs to work for longer, and our immune systems to beat diseases without killing all the cells —”good” and “bad”—in our bodies.