Last week, Penn’s Institute on Aging co-hosted its annual Sylvan M. Cohen lecture and poster session. This year, in partnership with the Abramson Cancer Center‘s Tumor Biology Program, the event focused on “protecting the genome in the longevity revolution: cancer and aging.” Brian Duke, Pennsylvania Secretary for Aging, set the stage for the day, encouraging Penn Medicine’s national experts in aging, Alzheimer’s and cancer in attendance to look to improve quality of life for the aging . “May today lead to breakthroughs,” Duke said.
The “wonder of discoveries to be presented today,” as co-host Chi Van Dang, MD, PhD, director of the Abramson Cancer Center, described, started with an intriguing Sylvan M. Cohen lecture by this year’s Visiting Scholar, Norman Sharpless, MD, from the Lineberger Comprehensive Cancer Center at the University of North Carolina.
Dr. Sharpless presented a compelling collection of research focused on the cancer and aging hypothesis. The expression of the p16 gene is important in cellular senescence, or cellular aging, he noted. This gene, p16, prevents cells from replicating, which can be good or bad. It can prevent cancer cells from replicating, but it can also halt useful cells from replicating. For instance, beta cells in the pancreas need to constantly replicate to keep up the ability to produce insulin. When there isn’t enough insulin produced, Type 2 Diabetes occurs. So, while halting P16 expression keeps cancers at bay, over time, the lack of production of other cells can lead to cellular aging.
Noting that there are multiple genetic hotspots in regions related to inflammation and senescence, Dr. Sharpless suggested “thinking about atherosclerosis and autoimmune diseases as aberrant replication diseases, like cancer.”
Looking at environmental factors that may also contribute to aging, the researchers look for “gerontogenic” toxins and determined that smoking is one that will age you, and that others may include a high fat diet. The team is currently looking at the long term impact of other environmental factors, such as cancer treatments, to see if cellular aging is adversely impacted.
Following Dr. Sharpless’ lecture, Penn Integrates Knowledge (PIK) Professor Shelley Berger, PhD, representing the Perelman School of Medicine and the School of Arts and Sciences, opened up an in-depth conversation on epigenetic changes that occur in aging. During a follow-up Q&A, Dr. Berger conferred with Penn’s Joe Baur and Penn Memory Center’s Steve Arnold and reinforced the potential utility of a compound found in grapes, red wine and nuts called resveratrol, in age-related diseases.
Later in the day, a trio of presenters discussed additional aspects linked to the aging process:
- Penn’s F. Bradley Johnson, MD, PhD, discussed telomeres that connect aging to cancer. “As people get older, telomeres – the caps on the end of chromosomes – get shorter, causing dysfunction,” says Johnson.
- Abramson Cancer Center’s Eric Brown, PhD, talked about replication stress in cells and in aging.
- CHOP’s Douglas Wallace, PhD, contended that energy impacts systems related to aging diseases.
The interdisciplinary group gave lots of great ideas that experts from both the Institute on Aging and the Cancer Center’s Tumor Biology Program will take back and see how they can apply to their own areas of research.