Suzanne Cory
As a youngster, Suzanne Cory imagined her future self at a typewriter, concocting adventure stories. At age 12, she wrote Grey Gold, a novel in which children save their family from poverty when they discover ambergris on a beach. Although Cory loved language and the infinite worlds it could evoke, she moved toward biology, inspired in part by the opening moments of a university genetics lecture. The instructor charged into the room, electrified by what he had just learned: Each chromosome is made of a single DNA molecule. Cory absorbed his enthusiasm—and instantly fell in love with DNA. Eventually she headed to Francis Crick’s lab at the University of Cambridge, U.K. for her Ph.D. She needed financial support and learned that only one fellowship was available to women. She applied for it and got the award.
While in England, Cory met her future husband and scientific partner, Jerry Adams. After setting up their lab in Australia, they imported the then-new technology of genetic engineering. With it, they probed questions about antibody diversity and production. They demonstrated, for instance, that cells cut and paste antibody-gene segments to engineer the precise immune response the body needs at each point during an infection.
Around that time, crucial findings that captured Cory’s imagination were emerging from other labs. She learned that cancer-causing viral genes resemble DNA sequences from host cells—and that improper activation of these normal genes can provoke uncontrolled growth. Furthermore, she read that cells from Burkitt lymphoma—a malignancy of antibody-producing cells—carry a characteristic DNA swap, or translocation, between two chromosomes.
Knowing from her work on antibody-gene rearrangements that lymphocytes like those that give rise to Burkitt lymphomas excel at DNA reshuffling, she wondered whether sloppiness during that process had placed part of an antibody gene alongside one that can spur cell division. In 1983, she and Adams found exactly that situation in Burkitt tumors: A gene that provokes cancer when inappropriately triggered, myc, had moved next to antibody-gene sequences.
Eager to test whether such fusions can cause cancer, Cory, Adams, and collaborators engineered mice to carry myc linked to antibody-gene elements that turn on genes. In 1985, they reported that these animals develop lymphomas. This observation suggested that overzealous myc in Burkitt cells promotes malignant growth.
During these studies, Cory detected numerous hints that additional genes contribute as well. She went on to study several other cancer-causing genes that are roused by chromo chromosome translocations and—with Adams and Ph.D. student David Vaux—discovered that one, bcl-2, helps cells survive under conditions that normally incite death. Misbehaving cells usually self-destruct, which ensures the organism’s health. Overactive bcl-2 thwarts this process. By creating mice that carry a version of this gene that is always on, Cory and her colleagues showed that it speeds myc’s ability to cause cancer. Cory thus established that genes can foster malignancies not only by encouraging cell proliferation, but also by blocking cell death. Instead of killing themselves, marred cells that inappropriately stimulate bcl-2 and its kin persist long enough to accumulate additional genetic damage that sparks unrestrained duplication.
Author: Evelyn Strauss, Ph.D.