Mari Lowe Seminar Series - Suzanne J. Baker, PhD
New Bolton Center Kennett Square, PA
Emergencies & Appointments:
Ryan Hospital Philadelphia, PA

Mari Lowe Seminar Series - Suzanne J. Baker, PhD

Suzanne J. Baker, PhD
  • 4:00 PM –5:00 PM
  • Address: 380 S. University Ave.
  • Location: Philadelphia, PA
Suzanne J Baker, PhD-Mari Lowe Center for Oncology, Penn Vet

Mari Lowe Seminar Series

Title: “Transforming Chromatin: Oncogenic Histone H3 Mutations in Diffuse Intrinsic Pontine Glioma"

  • SpeakerSuzanne J. Baker, PhD
    • Director, Brain Tumor Research Division
    • Associate Director, Basic Research, Comprehensive Cancer Center
    • Co-Leader, Neurobiology & Brain Tumor Program
    • Endowed Chair in Brain Tumor Research
  • Date: Thursday, February 20, 2020
  • Time: 4 pm 

Refreshments will be available.

130 Hill Pavilion
University of Pennsylvania School of Veterinary Medicine
380 S University Avenue, Philadelphia, PA 19104 

About Dr. Baker's Research:

The laboratory is focused on elucidating the mechanisms driving diffuse high-grade glioma (HGG) in children. In children and adults, diffuse high-grade gliomas (HGGs), including Grade III anaplastic astrocytomas and Grade IV glioblastomas, share a devastating outcome, with median survival slightly greater than one year, and five-year survival of 10-25%. Although HGGs from different age groups share related gene expression signatures, histopathological features, and frequent mutations in common pathways, there are a number of distinguishing features of pediatric HGG that indicate a unique pathogenesis. While adult glioblastomas arise predominantly in the cerebral cortex, in children, a broader spectrum of anatomical locations are more frequently involved, including the occurrence of diffuse intrinsic pontine gliomas (DIPGs), which arise in the brainstem.

Recent genome-wide studies from our group and others provided abundant evidence that unique selective pressures drive HGG in children compared to adults, identifying novel oncogenic mutations connecting tumorigenesis and chromatin regulation as well as developmental signaling pathways. It is now clear that there are at least several distinct subgroups of pediatric diffuse HGG based on clinical features and recurrent mutations. Ongoing work is directed towards integrating the latest genomic findings from primary human tumors to develop improved models of these disease subgroups that recapitulate the genetic and biological features of the disease for mechanistic studies and preclinical testing of selective therapies.

Shivani Berry