Lab study links a protein called VCAM1 to glioma growth
Original title: Vascular Cell Adhesion Molecule 1 Is Associated With Immune Remodeling, Glioma Progression, and Tumor Cell Survival in U87 and U251 Cells.
How far along is this research?
- Lab cells
- Animals
- Review
- Tested in people
This was done on cells in a lab, not in people. It is a very early step.
This was lab work on cells in a dish and on stored data, not a treatment given to people.
The short version
Early lab work hints that a protein called VCAM1 helps glioma: A tumor that starts in the glial cells. Those are the support cells of the brain and spinal cord. Gliomas are given a grade from 1 to 4. The grade says how the tumor is expected to act. See the glossary cells stay alive.
What was studied. Researchers looked at stored gene and protein data from people with glioma: A tumor that starts in the glial cells. Those are the support cells of the brain and spinal cord. Gliomas are given a grade from 1 to 4. The grade says how the tumor is expected to act. See the glossary. They also blocked a protein called VCAM1 in two glioma cell lines grown in a dish.
What they found. VCAM1 levels were higher in glioma: A tumor that starts in the glial cells. Those are the support cells of the brain and spinal cord. Gliomas are given a grade from 1 to 4. The grade says how the tumor is expected to act. See the glossary tissue than in normal brain tissue. Levels went up as tumors reached a higher grade. People with higher VCAM1 levels lived a shorter time. When the team blocked VCAM1 in the cells, more of those cells died.
What this means, and what it doesn't
What it could mean: VCAM1 might someday help doctors tell how risky a tumor is. It may also point to a target for future drugs. Right now it does not change any treatment.
What it doesn't mean: This is not a new treatment. The work was done on cells in a dish and on stored patient data. No one was given a drug in this study. It is not a cure, and it is many years away from everyday care.
Source: PubMed, October 21, 2026 · Read the original
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