Understanding Molecular Mechanisms of Glioma-Glial Cell-Cross Communication

Authors

• Lauren Dain, Virginia Commonwealth University

Original Publication Date

2026

Document Type

Presentation

Comments

12th Annual VCU 3MT® Competition, held on October 9, 2026.

Abstract

Glioblastoma survival rates have remained under 18 months for 40 years due to complex, redundant signaling within the tumor microenvironment. Using a mouse model, this research investigates how glioblastoma cells communicate with neighboring non-cancerous cells, specifically astrocytes. Findings reveal that tumor cells release signaling molecules causing astrocytes to express elevated heat shock protein 27 (HSP27), a protein critical to cell survival. Interrupting this intercellular support network aims to weaken tumor viability and advance targeted therapeutic strategies for brain cancer.

Accessibility Note

Content is digitally accessible 2026

Transcription

From the School of Medicine, Lauren Dain, Understanding Molecular Mechanisms of Glioma-Glial Cell-Cross Communication. Their advisor is Dr. Tomasz Kordula. Good afternoon, everybody. I bet several of us love a good jigsaw puzzle. And when you're working on a big puzzle, maybe 1,000, 2,000 pieces, those pieces can occupy your dining room table for a week or a month. Now imagine that puzzle is on your table for 40 years where you're making no significant progress. And as you continue to make no progress, people continue to die. Unfortunately, studying glioblastoma can feel a lot like this scenario. Glioblastoma is a very aggressive cancer that forms in the brain. And although patients can be treated with surgery, chemotherapy, and radiation, the average patient survival is less than a year and a half. And that number has not increased in the last 40 years. This is a patient population that deserves more answers and better therapies. But studying glioblastoma is really complicated. Tumors are not just made of tumor cells, here in red and here in green. That would be way too easy, wouldn't it? It's also made of all these other cell types as well. And all these cells communicate with and influence one another in ways that are not completely understood. They also all support tumor growth in many ways. And a lot of these functions are redundant, meaning that if we target one pathway, another will likely take its place. So my research uses a mouse model of glioblastoma. I can put mouse glioblastoma cells into the brain, allow them to grow under different conditions, and see which changes affect how these cells interact. With this model, I can study tumor tissue both from the mouse brain as well as cells in a dish. So, in a current project, I have found that glioblastoma cells release a molecule which is taken up by astrocytes, these green cells along the edge, and causes them to make high levels of an important protein called heat shock protein 27. Now, in a bunch of different kinds of cancer cells, we know that this protein is really important for their survival. But does it do the same thing in supportive cells? Now that we've nearly identified the whole mechanism, the question is now why? What is it that heat shock protein 27 is doing in these astrocytes? The goal of this research is to interrupt this communication, decrease the amount of support that tumors receive, and one day develop therapies that will finally push the needle forward for patient survival. So as we continue to put our pieces into the puzzle, the hope is that one day we will step back and finally see the whole picture. Thank you.

Rights

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