Dr Robert Vonderheide
Director, Abramson Cancer Center, Perelman School of Medicine, University of Pennsylvania; Vice Dean, Cancer Programs, Perelman School of Medicine; Vice President, Cancer Programs, University of Pennsylvania Health System, John H. Glick, MD, Abramson Cancer Center Director’s Professor; Lead Physician for the Cancer Service Line of the Health System.
Dr. Vonderheide graduated from the University of Notre Dame (Chemical Engineering) and obtained his DPhil in immunology from Oxford University as a Rhodes Scholar. He graduated from Harvard Medical School and completed a residency in Internal Medicine at the Massachusetts General and a fellowship in medical oncology at the Dana Farber. As an NIH-funded investigator at Penn Medicine, Dr. Vonderheide directs a research team focused on cancer immunology and immunotherapy. He has published more than 160 peer-reviewed manuscripts with senior-author papers in high-impact journals such as Science, Nature, Cancer Cell, and the New England Journal of Medicine. He is well-known for deciphering the immune mechanisms of CD40 activation in cancer and directing clinical trials of novel immunotherapy.
Nationally, Dr. Vonderheide is a member of the National Cancer Institute Board of Scientific Advisers, the National Comprehensive Cancer Network Board of Directors, and serves on the scientific advisory boards of seven NCI cancer centers. He is an elected member of the American Society of Clinical Investigation (serving on the ASCI council from 2014-2017) and American Association of Physicians.
As Vice Dean and Vice President for Cancer Programs, Dr. Vonderheide is responsible for setting the vision for cancer care and research, securing funding and resources, facilitating team-based transdisciplinary research, and decision-making on scientific policy, strategic directions, and investments. He oversees Abramson Cancer Center’s Research Programs and Shared Resources, and the Cancer Center’s systems for Clinical Protocol and Data Management, Community Outreach and Engagement, Cancer Education and Training, and Administration.
Case for priming not checkpoint in cancer immunotherapy of pancreas cancer
Most tumours are unresponsive to immune checkpoint blockade, especially if deep immunosuppression in the tumour develops prior to and prevents T cell immunosurveillance. Failed or frustrated T cell priming often needs repair before successful sensitization to PD-1/PD-L1 blockade. CD40 activation plays a critical role in generating T cell immunity, by activating dendritic cells, and converting cold tumours to hot. In preclinical studies, agonistic CD40 antibodies demonstrate T cell-dependent anti-tumour activity, especially in combination with chemotherapy, checkpoint inhibitory antibodies, and other immune modulators. With the advent of multiple CD40 agonists with acceptable single-agent toxicity, clinical evaluation of CD40 combinations has accelerated.
Video of Keynote Talk Slides Only