Kalish Laboratory

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The Kalish Lab studies how genetic and epigenetic alterations lead to overgrowth syndromes. This work focuses largely on patients with Beckwith-Wiedemann syndrome (BWS) and understanding the transition from normal growth to overgrowth to tumor formation.

BWS is the most common cancer predisposition and growth disorder that leads to cancer in children. Children with BWS can develop overgrowth of a number of different organs and in some cases develop tumors, most commonly hepatoblastoma (liver cancer) and/or Wilms tumor (kidney cancer). Some of the same genetic and epigenetic changes that cause BWS are also seen in other types of cancer; therefore studying BWS is a window into understanding the larger questions about growth and the transition to cancer.

The Kalish Lab focuses on improving clinical care for children with BWS through clinical and translational research. The lab oversees the BWS registry and biorepository and its work uses clinical data and samples to understand the transition between normal growth, overgrowth, and cancer.

The lab’s clinical research focuses on improving care for the clinical features of BWS and understanding the correlations between those manifestations. Through this work the lab continues to develop national management guidelines for BWS. Its translational research focuses on how the epigenetic and genetic changes lead to the features of BWS including overgrowth and cancer, with goals of understanding these mechanisms and developing therapeutics.

Project Highlights

  • Understanding the epigenetic landscape on chromosome 11
  • Defining global expression signatures in overgrowth syndromes
  • Defining the mechanism of tumor formation in BWS
  • Developing cell-based models of BWS
  • Treating macroglossia (enlarged tongue) in BWS 
  • Investigating the utility of cancer screening in BWS
Leader
Jennifer M. Kalish

Jennifer M. Kalish, MD, PhD

Director, Beckwith-Wiedemann Syndrome Program of Excellence
Dr. Kalish's research focuses on understanding the molecular and epigenetic mechanisms that contribute to the predisposition to cancer that is characteristic of pediatric patients with rare imprinted gene disorders, including the overgrowth disorder Beckwith-Wiedemann syndrome (BWS).