About Dr. van Deursen

Jan van Deursen, Ph.D., received his Bachelor of Science in biology from the University of Nijmegen in the Netherlands, and continued at that institution to earn his master's degree and doctorate in molecular and cellular biology.

In 1994, Dr. van Deursen started his independent research career as a faculty member at the St. Jude Children's Research Hospital in Memphis, Tennessee. During the next five years, he conducted research in his laboratory, elucidating the mechanisms that underlie nuclear-cytoplasmic transport and how regulation of this process contributes to leukemia. He also developed a mouse gene knockout core facility.

In 1999, Dr. van Deursen was recruited to the Department of Pediatric and Adolescent Medicine at Mayo Clinic, where he again developed and continues to direct an effective mouse gene knockout core facility. His research program investigates far-ranging topics such as the role of aneuploidy in development of cancer and the molecular mechanisms that contribute to aging. His work has been published in top journals, including Nature, Science and Cell, and is widely cited.

One of Dr. van Deursen's notable discoveries originated from work published in 2004, when his group generated a new mouse strain defective in chromosome replication due to reduced cellular levels of the spindle assembly checkpoint protein BubR1. Dr. van Deursen's lab found that these mice aged much more quickly than normal, dying of old age before they were one year old. Normal mice live 2.5 to three years.

In studying these mice, Dr. van Deursen's lab discovered that the animals showed rapid development of prematurely senescent cells — that is, cells that had turned on the p16 cell cycle inhibitor gene (INK4A), which made them stop dividing and begin to secrete inflammatory cytokines. To determine whether the senescent cells were not just indicators that the mice were aging rapidly but might actually be causing the rapid aging, fast-aging mice were crossed to mice that lacked the p16 gene.

The lab found that the cross-bred mice no longer suffered from the rapid development of age-associated syndromes, including poor vision from cataracts and loss of muscle and fat. This finding verified the hypothesis that the relatively rare senescent cells in tissues were somehow causing the surrounding normal cells to decay and develop problems associated with old age.

Next, in collaboration with the research group of James L. Kirkland, M.D., Ph.D., Dr. van Deursen's lab developed a different strategy to specifically remove the problematic senescent cells from mice. They generated a special transgenic strain of mice that would delete senescent cells if they were exposed to a specific drug. Dr. van Deursen's and Dr. Kirkland's labs found that this treatment not only removed the senescent cells but also prevented the rapid aging in these mice.

The team's work was published in Nature in November 2011 and captured the imagination of many in the scientific community as well as the public. Here, for the first time, was a clear demonstration of an intervention that dramatically delayed the deleterious effects of aging on multiple organs in a mouse model, in a way that, at least conceptually, could eventually be applied to humans.

In addition to generating a large number of exciting new projects in Dr. van Deursen's laboratory, this discovery has also prompted other scientists to begin studying the role of p16 and cellular senescence in mouse and human aging. As a concrete demonstration of the importance of this discovery, the journal Science selected the lab's Nature paper as one of the top 10 discoveries of the year in 2011.

In addition to Dr. van Deursen's scientific accomplishments, he is very active as an educator, having mentored more than 60 students, residents, postdoctoral fellows and junior faculty members. He has a strong commitment to supporting the successful careers of young upcoming scientists.

Dr. van Deursen has been recognized by numerous awards. He is the Vita Valley Professor of Cellular Senescence and was Mayo Clinic Investigator of the Year for 2012. He hopes that one day centenarians will be qualifying for the Boston Marathon.