Patients with high grade gliomas (HGG) face considerable treatment challenges and comprehensive research is needed to find new therapeutic options. Using the Pediatric Brain Tumor Atlas, researchers will identify genes that are expressed differently in patient-derived tumor samples compared to normal tissue samples. Gene expression, the process by which the genetic information is used to direct production of proteins in the body, is crucial in understanding the similarities and differences across tumor types. Additionally, these genetic signatures will be used in comparison to lab-grown tumor cell lines that have been genetically manipulated or treated with various drugs. Researchers hope to analyze these comparisons and identify patterns in gene expression that could pave the way for the development of new therapies.
What are the goals of this project?
Researchers will identify and compare tumor samples, normal tissue samples, and lab grown tumor samples in an effort to identify patterns in gene expression.
What is the impact of this project?
The identification of patterns in gene expression across tumor types could lead to the development of new targeted therapies.
Why is the CBTN request important to this project?
The breadth and depth of data available through the Pediatric Brain Tumor Atlas will be pivotal in supporting this project.
The Children's Brain Tumor Network contributed to this project by providing access to the Pediatric Brain Tumor Atlas.
- Dr. Jay Kalin from Johns Hopkins
- Dr. Federica Piccioni of the Genetic Perturbations Platform group at the Broad Institute
Jamie Anastas, PhD
Dr. Anastas is studying how mutations in chromatin-associated factors affect heterochromatin organization in pediatric cancer.
Boston Children's Hospital
Mariella Filbin, MD, PhD
Dr. Mariella Filbin is the Research Co-Director at Harvard Medical School. She received her MD and PhD in biochemistry and molecular biology from the Medical University of Graz, Austria. Following graduation she completed her pediatric residency at the Boston Children's Hospital and completed a fell
Harvard Medical School
David Root, PhD
Dr. David Root is the Senior Director of the Genetic Perturbation Platform and Functional Genomics Consortium at the Broad Institute of MIT and Harvard. He received his PhD in physical chemistry from Stanford University. He was previously assistant professor of physical chemistry at Swarthmore Colle
Philip Cole, MD, PhD
Dr. Phil Cole is a Professor of Medicine and Biological Chemistry and Molecular Pharmacology at Harvard Medical School. He received his MD and PhD from Johns Hopkins where he pursued research in bioorganiz chemistry. Following graduation he completed post-doctoral training at Harvard Medical School
Yang Shi, PhD
Yang Shi joined Harvard Medical School as an assistant professor in 1991 and was appointed a Professor of Pathology in 2004. He is currently a Professor of Cell Biology. He is also the Merton Bernfield Professor of Neonatology in the Division of Newborn Medicine at Children’s Hospital Boston. Yang
Harvard Medical School
Todd Golub, MD
Dr. Todd Golub is the Core Institute Member, Chief Scientific Officer, and Director of the Cancer Program at Broad Institute. He received his medical degree from the University of Chicago Pritzker School of Medicine. Following graduation, he completed his internship, residency, and fellowship traini
Jay Kalin, PhD
Federica Piccioni, PhD
High-grade Gliomas (HGG) or astrocytomas in children nearly always result in a dismal prognosis. Although novel therapeutic approaches are currently in development, preclinical testing has been limited, due to a lack of pediatric-specific HGG preclinical models. These models are needed to help test
Diffuse Intrinsic Pontine Glioma
A presumptive diagnosis of DIPG based on classic imaging features, in the absence of a histologic diagnosis, has been routinely employed. Increasingly however, histologic confirmation is obtained for both entry into research studies and molecular characterization of the tumor. New approaches with
Gene-22. Re-Programing Chromatin with a Bifunctional LSD1/HDAC Inhibitor Induces Therapeutic Differentiation in DIPG
Diffuse intrinsic high grade glioma (DIPG) is an almost universally fatal tumor of childhood characterized by epigenetic dysregulation driven by somatic H3.3/H3.1 K27M mutations observed in >80% of tumors. We conducted a chromatin-focused CRISPR screen and identified a novel strategy to inhibit the
Jamie Anastas, Mariella Filbin, Mirhee Kim, Jay Kalin, Barry Zee, Andres Blanco, Jayanta Das, Todd Golub, Philip Cole, Yang Shi