How did your interest in science develop?
My interest in science emerged early, as my favorite subjects in high school were math, physics, and chemistry. However, it wasn’t until I volunteered in an immunology lab at Scripps Research Institute during my first couple of summers home from college (at UC Berkeley) that I became thrilled by the complexities of biological problems. At UC Berkeley, my work as an undergraduate researcher in Dr. Robert Tjian’s lab launched my love of enzymes that manipulate nucleic acids, an interest that continued while I was a graduate student in Dr. Donald Rio’s lab (at Massachusetts Institute of Technology at the time) and then as a postdoctoral fellow with Dr. Bruce Stillman at Cold Spring Harbor Laboratory. Since then, my own lab at the UMass Chan Medical School — which uses molecular genetics, biochemistry, and genomic tools to investigate chromosome assembly and function in yeast and human cells — has been continually funded by the National Institutes of Health since 1997. Over the years, I have particularly enjoyed seeing members of my laboratory learn and grow as they make new discoveries.
Did you start off as a cancer researcher? If not, what led you to work on cancer-related research topics?
I hadn’t started my career with a specific focus on cancer. Instead, I had been focused on fundamental mechanisms of chromosome formation for most of my early career. Of course, our interest in basic chromosome biology naturally intersects with questions of genome stability. That is, when chromosome duplication goes wrong, the result is DNA damage that is a fundamental driver of carcinogenesis.
What cancer-related projects are you working on?
In earlier studies, we discovered that a human protein important for duplicating chromosomes also governs the three-dimensional localization of multiple proteins. One of these target proteins, Ki-67, is used extensively in the clinic as a marker to grade tumors, as extremely aggressive tumors express high levels of Ki-67. Despite the longstanding clinical utility of this marker, much less is known about the biological functions of Ki-67. We have shown that removal of Ki-67 triggers a transient delay in cell growth in normal cells, but not in most cancer cells. These data suggest that Ki-67 protects normal human cells and that this effect becomes muted in tumors. Therefore, we are keenly interested in learning how these signaling mechanisms work, because they will have broad implications for cancer biology.
What do you see as the most promising technology or techniques in cancer research right now?
Precise genome editing and advanced imaging techniques are synergizing to provide unparalleled resolution in recent studies.
What is your message to potential donors?
Many of the most transformative discoveries in heath science (for example, PCR, RNAi, CRISPR-Cas9) did not result from directed attempts at translational research. Having a broad research community with the intellectual freedom to pursue research on many fronts will always be key to progress.
About Paul D. Kaufman
Paul D. Kaufman, PhD, is a professor in the Department of Molecular, Cell and Cancer Biology at the UMass Chan Medical School. Dr. Kaufman obtained a PhD from Massachusetts Institute of Technology and received postdoctoral training at Cold Spring Harbor Laboratory.
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