Greehey CCRI Seminar Series – Fall ’26 John Powers, PhD (UT Austin)
John Powers, Ph.D.
Assistant Professor, Department of Pediatrics
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John Powers, Ph.D.
Assistant Professor, Department of Pediatrics
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John Powers, Ph.D., is an assistant professor of pediatrics at Dell Medical School and a CPRIT Scholar. Powers is a double alumnus of The University of Texas at Austin, where he received both his bachelor’s degree in microbiology and his doctorate in molecular genetics and microbiology. He completed his training at Harvard Medical School and Boston Children’s Hospital, where he worked in microRNA biology and cancer genetics. Prior to joining the Dell Pediatric Research Institute, he was a principal scientist at Moderna Therapeutics, where he led the cellular genetic engineering group.
One of the Powers lab’s main research efforts is focused on RNA biology and RNA-based therapeutics for pediatric neuroblastoma. Neuroblastoma, the group’s main focus, is a rare type of cancer that mainly affects children five years and younger. It spreads easily, and high-risk cases have a poor prognosis. Understanding the underlying genetic mechanisms driving this disease, through the lens of RNA function and expression networks, will enable the laboratory to pursue more robust RNA-based therapeutic targets for neuroblastoma and other cancers.
Additionally, the Powers lab has a strong interest in personalized cancer vaccines and is pursuing a novel, low-cost platform for patient delivery. Making vaccines tailored to an individual patient’s disease could lead to the development of disease-specific vaccine-based therapies, especially in cancers that currently lack targeted therapies.
In his research, Powers focuses on understanding the underlying genetic mechanisms leading to pediatric neuroblastoma, a rare type of cancer that forms in certain types of nerve tissue and often affects young children. Poor prognosis in neuroblastoma is frequently driven by a gene with the potential to cause cancer known as MYCN. Powers’ research focuses on improving the understanding of how this gene becomes amplified and dysregulated, a process that leads to neuroblastoma.