Research Spotlight: Suzanne Baker

Dr. Suzanne Baker: Helping Unlock the Biology of DIPG and DMG

For more than a decade, scientists have made remarkable strides in understanding what makes diffuse intrinsic pontine glioma (DIPG) and diffuse midline glioma (DMG) so different from other childhood brain tumors. Dr. Suzanne Baker has been at the forefront of many of those discoveries.

A leading pediatric brain tumor researcher at St. Jude Children’s Research Hospital, Dr. Baker has devoted much of her career to understanding the fundamental biology of childhood high-grade gliomas and using that knowledge to uncover new possibilities for treatment. Today, she serves as deputy director of the St. Jude Comprehensive Cancer Center, co-leader of its Neurobiology and Brain Tumor Program and Endowed Chair in Brain Tumor Research.

Her connection to ChadTough Defeat DIPG Foundation is equally significant. Dr. Baker chairs the foundation’s Scientific Advisory Council (SAC), a group of leading childhood brain cancer experts charged with reviewing grant applications and recommending the research projects with the greatest scientific promise.

A Discovery That Changed How We Understand DIPG and DMG

One of Dr. Baker’s most significant contributions came through research that helped identify mutations in proteins called histones in pediatric high-grade gliomas. Dr. Baker and her colleagues discovered that a mutation known as H3 K27M occurs in the majority of DIPG tumors. The discovery provided some of the first clear evidence that pediatric high-grade gliomas consist of biologically distinct subgroups and helped reshape how scientists understand and classify these tumors.

Histones act somewhat like spools around which DNA is wrapped, helping determine which genes a cell turns on or off. The H3 K27M mutation disrupts that process, altering the way genes are regulated. But identifying the mutation raised another important question: If it can disrupt cells throughout the body, why do these tumors develop predominantly in the brainstem and other midline regions of the brain?

That question has become an important focus of Baker’s research.

DIPG is now understood as part of the broader family of tumors known as diffuse midline glioma, or DMG. DIPG refers specifically to tumors arising in the pons, a region of the brainstem, while DMG can develop in other midline structures of the brain and spinal cord. Many of these tumors share underlying biological features, including changes involving H3 K27.

New Clues to Why DMG Develops Where It Does

In August 2026, Dr. Baker and her St. Jude colleagues published findings in Nature Communications that bring researchers closer to answering a longstanding question: Why does a mutation capable of affecting cells throughout the body lead to tumors primarily in the brainstem and other midline regions of the brain?

To investigate, Baker’s team studied oligodendrocyte precursor cells, or OPCs, which are developing brain cells that eventually help produce myelin, the protective insulation around nerve fibers. Researchers compared these cells from the brainstem, where H3.3 K27M-driven tumors frequently develop, with cells from a region of the brain where these tumors rarely occur.

They found something striking. Although the H3.3 K27M mutation altered DNA packaging in similar ways across both regions, its effects on the cells themselves were very different. In brainstem cells, the mutation kept cells in a younger, actively dividing state for a longer period of time. That extended window of immaturity may help create conditions that make the brainstem particularly vulnerable to DMG. The researchers also found that the mutation had a stronger effect on developmental signaling pathways in brainstem cells. 

The findings suggest that the mutation alone doesn’t tell the entire story. Where a cell originates and where it is in the developmental process may be just as important in determining whether that mutation ultimately contributes to cancer.

That deeper understanding could eventually have therapeutic implications. By identifying the developmental processes that DMG cells exploit to form and grow, researchers may uncover new vulnerabilities that can be targeted with treatment. As Baker explained, understanding how childhood cancers hijack normal development is critical to designing more effective therapies.

Guiding ChadTough Research Investments

Dr. Baker’s expertise also plays an important role in determining how ChadTough Defeat DIPG research dollars are invested.

As chair of the Scientific Advisory Council, she leads a group of experts who carefully evaluate grant applications for scientific merit and potential impact. Their recommendations help ensure donor dollars are directed toward the most promising DIPG and DMG research, from established investigators pursuing ambitious new ideas to early-career scientists bringing fresh perspectives to the field.

That process has become increasingly important as interest in DIPG and DMG research has grown. With more scientists bringing new ideas, technologies and approaches to the field, rigorous scientific review helps ChadTough Defeat DIPG identify where its funding can have the greatest potential impact.

For families who have watched research progress too slowly for far too long, scientists like Dr. Baker offer reason for hope. Each discovery adds another piece to an extraordinarily complicated puzzle. And with a better understanding of how these tumors begin, grow and survive comes greater opportunity to find ways to stop them.

Through both her own groundbreaking research and her leadership of the Scientific Advisory Council, Dr. Baker is helping ensure the science continues moving forward, bringing us closer to the breakthroughs children with DIPG and DMG desperately need.