Go Gray in May: Raising Brain Cancer Awareness

May 17th is recognized as the specific National DIPG Awareness Day, frequently highlighted during the broader "Go Gray in May" Brain Tumor Awareness Month to raise funds and awareness for Diffuse Intrinsic Pontine Glioma.

With Reed Day of Giving right around the corner, we invite employees to share their stories and favorite charities to spread awareness and give us a deeper sense of why we donate to certain causes. We have an employee who was brave enough to share their story and favorite charity, and why it holds deep personal significance. If you would like to donate to this cause during the Reed Day of Giving, go to the Cure Starts Now Foundation's website, visit The Cure Starts Now.

If you have a story or a charity you'd like to share and raise awareness for, send us an email at BUILD@Reed.net

What is Diffuse intrinsic pontine glioma (DIPG)?

Diffuse intrinsic pontine glioma (DIPG) is a fast-growing (aggressive) brain tumor that is hard to treat and primarily affects children between the ages of five and 10. DIPG grows within the part of the brain called the pons that controls major functions such as breathing, heart rate and motor control (dexterity). The pons, together with the medulla oblongata and the midbrain, form the brainstem. Anatomically, the brainstem is located at the base of the brain, slightly above the back of the neck, and connects the cerebellum and thalamus to the spinal cord.^1,2

As suggested by its name, DIPG is characterized by a high potential to spread (diffuse) into surrounding brain tissue.² Although DIPG tumors generally arise in the pons, they often spread into the surrounding tissues, particularly the cerebellum and thalamus as well as the spinal cord.^3,4 About 80% of brainstem tumors in children are DIPG tumors.

Due to its location in the brain, surgical resection of the tumor is generally not an option for DIPG, and radiation therapy (RT) remains the standard of care.⁵ DIPG is still incurable and is the leading cause of pediatric brain tumor-related deaths. The prognosis for children diagnosed with DIPG remains poor, with a median survival time of nine to 10 months and a very low likelihood of surviving beyond two years.^1-5

While no definitive date exists for the first documented diagnosis, evidence suggests probable cases dating back nearly a century. DIPG gained recognition in the 1960s when astronaut Neil Armstrong’s daughter, Karen (“Muffy”) passed away from the disease.

Before 2016, tumors were classified mostly by where they appeared in the brain. In 2016, the World Health Organization (WHO) started to classify tumors not just by location but by genetic variants, so a new category was introduced called “diffuse midline glioma, H3 K27M-mutant”. This category replaced terms like “DIPG”, so a diffuse intrinsic pontine glioma with an H3 K27M mutation was called “diffuse midline glioma, H3 K27M-mutant.”

In 2021, the WHO updated the term to “diffuse midline glioma, H3 K27-altered”⁶ as it became clear that not all tumors with similar biology had the exact same K27M variant and that there were some tumors that had other variants that caused the same effect. The new term “K27-altered” is broader and more inclusive.

While DIPG is no longer a formal diagnostic category in WHO classifications, it is still used clinically or descriptively to refer to tumors in the pons that have classic imaging features. If the tumor has the H3 K27 variant, the formal diagnosis is “diffuse midline glioma, H3 K27-altered”. Diffuse midline glioma, H3 K27-altered also applies to other midline tumors with similar variants.

Development of DIPG likely involves specific cells in the brain and is linked to certain genetic markers known as drivers of tumorigenesis. Among the markers now identified to be directly or indirectly associated with DIPG, a change (variant) on in one of the histones H3 genes is recognized as one of the most important determinants of poor prognosis. This mutation leads to a change in the amino acid sequence of the histone protein at position 27 known as the H3K27M. H3K27M refers to the amino acid lysine (K) being replaced with a methionine (M) at position 27 in the secreted (produced) protein.³

Histones have critical roles within all cells. They help pack the DNA within the nucleus of cells and play a role in the mechanism by which proteins in the cell are synthesized by controlling which genes are turned on or off (gene expression). Thus, any change in the amino acid sequence of one of the histones H3 genes can have a severe effect on how the cell controls the expression of certain genes.

To date, other DIPG genetic markers have been identified, and many intracellular pathways have also been shown to be affected by or involved in the development of DIPG, which are providing new insights towards new therapeutic approaches. In August 2025, dordaviprone (Modeyso) was approved by the U.S. Food and Drug Administration (FDA) for treatment of diffuse midline gliomas that have the H3K27M variant.

NORD gratefully acknowledges Marcelo Ramalho-Ortigao, DSc/PhD, Medical and Science Advisor, DIPG Advocacy Group, Marc Jr Foundation Board Member, for the preparation of this report.