For long, it was unclear what drives aging at a molecular and cellular level. We know now that virtually all our cells accumulate damage as we age and this can eventually cause them to become ‘senescent’. Senescent cells cease to divide, but chronically secrete a wide range of factors that permanently alter their environment.
Dr. Peter de Keizer will delve into the background of his research on eliminating senescent cells. This has achieved remarkable results in mice, at least allowing for a spark of hope that this may be some day applicable to humans. And he might lift a corner of how, despite hurdles from institutes and regulatory bodies, individual researchers can -and maybe should- take the lead in translating their science to benefit society.
About Peter de Keizer
In 2009, biomolecular scientist Peter de Keizer obtained his PhD at Utrecht University. He studied the regulation of FOXO proteins under conditions of stress and their role in tumor suppression. During these years, he identified FOXOs as targets in oncogene and damage-induced senescence. Being highly intrigued by cellular senescence, he joined the lab of a pioneer in the field, Prof. dr. Judith Campisi, at the Buck Institute for Research on Aging, in Novato, CA, USA.
In 2012, Peter joined the Erasmus Medical Center in Rotterdam, where he designed the third generation of anti-senescence drugs: the FOXO4-DRI peptide, aka Proxofim. This proved to be effective in counteracting signs of chemotoxicity and, excitingly, was able to restore certain healthspan features in models for fast and natural aging. This research on mice received worldwide media attention, including extensive coverage in ‘De Volkskrant’.
In January 2018, Peter joined the University Medical Center Utrecht as assistant professor, where his group will be focused on identifying the molecular variation in individual senescence phenotypes and how senescence dictates (cancer) stemness, cancer metastases and therapy resistance. In parallel the group is highly dedicated to develop the next generation of anti-senescence drugs with an improved safety profile to allow for human translation.