Fred and Suzanne Biesecker Pediatric Liver Center

The Fred and Suzanne Biesecker Center for Pediatric Liver Disease is a world leader in the diagnosis and treatment of acute and chronic pediatric liver diseases. The Center’s aim is to provide the most skilled, compassionate, and state-of-the-art care available in a highly specialized environment that focuses on children and families and puts patient care and safety first.

Biesecker Pediatric Liver Center physicians and scientists are internationally recognized leaders in laboratory and clinical research on pediatric liver disease. The Center is a leading recipient of funding from the National Institutes of Health and other organizations. As a major referral center caring for a large number of children each year, the center is able to draw upon its vast pool of data for cross-collaborative research efforts with leading researchers in all areas of pediatrics.

The Center’s research programs aim to understand the mechanisms involved in the etiology and progression of pediatric liver diseases as well as the role of the immune system in the possible cause and ongoing damage in these diseases. Center investigators aim to explore and identify issues related to transplant immunobiology, regeneration (including engineering new liver cells), and injury in pediatric recipients undergoing liver transplantation. Additional goals include identifying genes implicated in pediatric liver diseases; identifying the basis for bile duct development, proliferation, and destruction in embryonic and larval zebrafish and mammals; identifying the genetic mechanisms of liver and biliary development in mammals; and understanding the mechanisms of liver fibrosis to identify approaches to prevent and treat it.

The Center’s research related to Alagille syndrome is focused on improving the mutation detection rate; understanding what factors influence the variability of severity (i.e. studying genetic modifiers); and understanding the spectrum and nature of vascular anomalies and how the Jagged-1 and NOTCH2 proteins interact with other cellular proteins and lead to the abnormalities seen in this syndrome.