Research Spotlight: Prateek Thenge

Fighting DIPG One Engineered Cell at a Time

I’m a PhD candidate in Molecular Pharmacology and Therapeutics at the University of Minnesota and a Predoctoral Fellow of the ChadTough Defeat DIPG Foundation.

I study DIPG, diffuse intrinsic pontine glioma. If you don’t know that name, I hope you never need to. It’s a devastating brain tumor that primarily affects children, growing deep within the brainstem where it cannot be safely removed. Today, there is no cure. Radiation may buy a few months, but for most families, a DIPG diagnosis marks the beginning of an unimaginable journey.

My research focuses on a unique type of immune cell called a gamma delta T cell. Unlike conventional T cells, which rely on HLA molecules—the body’s cellular “ID cards”—to identify threats, gamma delta T cells recognize stress signals that cancer cells struggle to hide. This is especially important in DIPG, where tumors often reduce HLA expression specifically to evade immune detection. Gamma delta T cells can see through that disguise.
I then engineer these cells further, equipping them with chimeric antigen receptors, or CARs. These synthetic receptors act like molecular GPS systems, directing immune cells toward specific proteins found on tumor cells. Traditional CAR-T therapies typically target a single protein, which can be effective until the tumor adapts and stops expressing that target. When that happens, the therapy loses its ability to recognize the cancer. Our approach is designed to make escape more difficult.

Instead of targeting one protein, we engineer cells to recognize two tumor-associated proteins simultaneously: B7-H3 and HER2. Both are highly expressed in DIPG and largely absent from healthy brain tissue. If a tumor loses one target, the engineered cell can still recognize the other, maintaining its ability to attack the cancer. At the same time, I use multiplex genome-editing tools to reprogram the cells internally, reducing the molecular signals that cause immune exhaustion within the tumor microenvironment. The goal is not only precision, but persistence—immune cells engineered to keep fighting long after conventional cells would have stopped.

Most of my days aren’t glamorous. I thaw cells. I count them. I run assays, troubleshoot failed experiments, and spend hours staring at data trying to understand what went wrong—only to start again the next day.

Science rarely moves in breakthroughs. Most of the time, it moves in millimeters. But every millimeter matters.
Because enough millimeters become a discovery. A discovery becomes a clinical trial. And a clinical trial can become more time for a child.

What keeps this work from becoming a never-ending series of experiments are the people behind it. My fellowship is a daily reminder that behind every cell line, every mouse model, and every graph is a child and a family living through something unimaginable.

Many of the families who support this research have experienced profound loss. Yet they continue to invest in science because they believe another family deserves a different outcome. They choose to transform grief into progress, heartbreak into hope.

That trust is the most humbling gift I have ever been given.

It also comes with responsibility. “Good enough for a publication” is very different from “good enough for a child in a clinical trial.” I never allow myself to forget that distinction. My goal is simple, even if the science is not: I want DIPG to stop being a death sentence. I want it to become a disease that medicine knows how to treat. I am only one person working on one piece of a very large puzzle. But I believe deeply in what we’re building: engineered immune cells derived from healthy donors, precisely targeted and designed for endurance. I believe this work has the potential to change what is possible for children facing this disease.

None of it happens without the families who turn their worst moments into momentum for someone else’s future.
Every experiment I run is guided by a single question: Could this one day give a family more time together? I intend to spend my career helping answer that question with yes.