Vanderbilt Prize lecturer Amon driven to solve genetic mysteriesFeb. 7, 2019, 9:28 AM
by Bill Snyder
For much of her career, Angelika Amon, PhD, recipient of the 2018 Vanderbilt Prize in Biomedical Science, has pursued a mystery with life-or-death consequences.
How does a normally lethal condition known as aneuploidy — having too many or too few chromosomes — enable some tumors to spread aggressively through the body? How are they able to hide from the immune system, which normally targets and destroys aneuploid cells?
Solving this mystery could lead to a new approach to cancer treatment. But it won’t be easy. “That’s the problem of aneuploidy,” Amon told a Vanderbilt audience last week. “The short answer is, it’s complicated.”
Amon is the Kathleen and Curtis Marble Professor in Cancer Research and professor of Biology at the Massachusetts Institute of Technology. She is the 13th recipient of the Vanderbilt Prize, which was established to honor exceptional women scientists who also have made significant contributions to mentoring other women in science.
Her talk, part of the Flexner Discovery Lecture Series, was sponsored by the offices of the Executive Vice President for Research of Vanderbilt University Medical Center, Jennifer Pietenpol, PhD, and the Dean of Basic Sciences of Vanderbilt University School of Medicine, Lawrence Marnett, PhD.
In her introductory remarks, Pietenpol, who also directs the Vanderbilt-Ingram Cancer Center, said Amon “personifies the essence of the Vanderbilt Prize.”
“She’s a pioneer in the field of genome maintenance, which has advanced our understanding of how abnormalities in cell division contribute to the development of cancer,” Pietenpol said. And “she’s unwavering in her support of women in science.”
Pietenpol also introduced Alissa Guarnaccia, the 2018 Vanderbilt Prize Student Scholar, a PhD candidate in the Department of Cell and Developmental Biology at Vanderbilt who will be mentored by Amon.
In her lecture, Amon described how aneuploidy causes multiple forms of genome instability, including defective DNA repair. “Obviously if you’re too unstable, you’ll die,” she said. But “just a little bit” of instability can accelerate tumor evolution.
How do these abnormal cells evade the immune system? “That’s a great teaching lesson,” Amon said. “If something doesn’t make sense, it’s trying to tell you something. We’ll just have to do the experiment.”