RESEARCHER SPOTLIGHT: TARA BARRON, PHD
CHADTOUGH DEFEAT DIPG FOUNDATION’S FELLOWSHIP GRANTING PROGRAM
Written by Jane Gresser, Volunteer Writer
ChadTough Defeat DIPG Foundation is fighting DIPG head on with its Fellowship Grants, designed to attract promising scientists to choose a career in DIPG research. Tara Barron, Ph.D., of Stanford University is a recent recipient of this grant. Dr. Barron is a fellow in the lab of Michelle Monje-Deisseroth, M.D., Ph.D. In a recent interview with Dr. Barron, we learned about recent advances in understanding the role of neuronal activity on DIPG tumor growth and how understanding the mechanism of commonly used neurologic medications may lead to therapies that improve and extend the lives of children with DIPG.
NEURONAL ACTIVITY DRIVES DIPG PROGRESSION
The goal of this research is to reveal insight into the active communication between neurons and DIPG cells to shift the view of DIPG from an isolated disease to an active and integrative system, and then to leverage these findings for more effective therapeutic strategies. Recent work has demonstrated that DIPG growth is powerfully driven by neuronal activity. It is known that some neurologic medications, like those that reduce anxiety and nausea (commonly given to children with DIPG), work by decreasing neuronal activity. The mechanism of some of these drugs works by increasing the transmission of a neurotransmitter called GABA, which has the effect of inhibiting neuronal activity. This suggests the possibility that use of medications that increase GABA signaling (also referred to as GABAergic) may inhibit DIPG tumor growth in children. Conversely, it is also possible that DIPG cancer cells may be interacting directly with GABA, which could lead to either progression or regression of DIPG tumor growth.
CAN EXISTING NEUROLOGIC MEDICATIONS IMPACT DIPG?
Dr. Barron’s research examines the relationship between neurons in the brain and DIPG tumor cells. Specifically, her work aims to determine the role of neuron-to-glioma GABA signaling in DIPG and learn how it affects DIPG tumor growth. Thus far, Dr. Barron and her team have learned that DIPG cells receive communication from GABAergic neurons and that drugs that target GABA signaling, such as anti-epileptic drugs and other neurologic drugs, can impact tumor growth. Her work with animal models of DIPG has demonstrated that some of these drugs promote tumor growth, while others reduce tumor growth leading to increased animal model survival. These exciting findings have therapeutic potential for DIPG patients.
Once her work is completed, she hopes the findings will inform decisions on which medications that impact GABA signaling should be given to DIPG patients to reduce tumor growth and which commonly used drugs to treat anxiety and nausea should not be given to DIPG patients at the risk of promoting tumor progression. Her hope is that this will extend and improve the lives of children with DIPG.
IMPORTANCE OF PRIVATE FUNDING FOR DIPG
“Private funding, including the research grants funded by ChadTough Defeat DIPG, are critical for moving the field of DIPG forward,” said Dr. Barron. “Foundations that specifically fund DIPG research not only enable but encourage researchers to include DIPG as a primary focus of their research.”
Progress continues to be made in DIPG treatment options. Over the past 10 years, the increased use of patient-derived DIPG cells in DIPG research has enabled researchers to quickly screen therapeutic strategies, which has led to novel upcoming treatment options such as immunotherapies and chemotherapies. DIPG research, such as that funded by ChadTough Defeat DIPG, will continue to uncover innovative ways to treat DIPG and improve the lives of DIPG patients.