Penn’s Institute on Aging recentlyco-hosted its annual Sylvan M. Cohen lecture and poster session. This year, inpartnership with the Abramson CancerCenter‘s TumorBiology Program, the event focused on “protecting the genome in thelongevity revolution: cancer and aging.” BrianDuke, Pennsylvania Secretary for Aging, set the stage for the day,encouraging Penn Medicine’s national experts in aging, Alzheimer’s and cancerin attendance to look to improve quality of life for the aging . “May todaylead to breakthroughs,” Duke said.
The “wonder ofdiscoveries to be presented today,” as co-host ChiVan Dang, MD, PhD, director of the Abramson Cancer Center, described,started with an intriguing Sylvan M. Cohen lecture by this year’s VisitingScholar, NormanSharpless, MD, from the Lineberger Comprehensive Cancer Center at theUniversity of North Carolina.
Dr. Sharplesspresented a compelling collection of research focused on the cancer and aginghypothesis. 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 itcan also halt useful cells from replicating. For instance, beta cells in thepancreas need to constantly replicate to keep up the ability to produceinsulin. When there isn’t enough insulin produced, Type 2 Diabetes occurs. So,while halting P16 expression keeps cancers at bay, over time, the lack ofproduction of other cells can lead to cellular aging.
Noting that thereare multiple genetic hotspots in regions related to inflammation andsenescence, Dr. Sharpless suggested “thinking about atherosclerosis andautoimmune diseases as aberrant replication diseases, like cancer.”
Looking atenvironmental factors that may also contribute to aging, the researchers lookfor “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 atthe 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 ShelleyBerger, PhD, representing the Perelman School of Medicine and the School ofArts and Sciences, opened up an in-depth conversation on epigeneticchanges that occur in aging.During a follow-up Q&A, Dr. Berger conferred with Penn’s Joe Baur, from the Department of Physiology and theInstitute for Diabetes, Obesity and Metabolism, and Penn Memory Center’s SteveArnold 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, atrio 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 Family Cancer Research Institute’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.
Theinterdisciplinary group gave lots of great ideas that experts from both theInstitute on Aging and the Cancer Center’s Tumor Biology Program will take backand see how they can apply to their own areas of research.