A surface protein works differently in radiation-resistant brain tumor cells
Original title: Collagen-dependent DDR1 ectodomain shedding regulates proliferative signaling in radiation-resistant glioblastoma.
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, not a treatment given to people.
The short version
This is early lab work on why some glioblastoma: A glioma that is given grade 4. Grade 4 is the highest grade there is. The tumor grows fast. Treatment usually starts soon after it is found. It often means surgery, and then radiation and chemotherapy. See the glossary cells keep growing after radiation.
What was studied. Researchers used glioblastoma: A glioma that is given grade 4. Grade 4 is the highest grade there is. The tumor grows fast. Treatment usually starts soon after it is found. It often means surgery, and then radiation and chemotherapy. See the glossary cells taken from patients. One set still responded to radiation. The other set had been made resistant to it. Both were grown in a gel made of collagen, and the team watched a surface protein called DDR1.
What they found. The resistant cells made more DDR1, but less of it was switched on. More of it was being cut off and shed from the cell surface. An enzyme called ADAMTS1 was much higher in the resistant cells. When the team lowered that enzyme, more whole DDR1 stayed on the cells and growth signals went up.
What this means, and what it doesn't
What it could mean: This adds to what scientists know about how tumor cells change after radiation. It may point to new things to study later. It does not change any treatment a patient can get now.
What it doesn't mean: This does not mean a new treatment. The work was done on cells grown in a dish, not in people. No one was treated, and no patient results were measured. It is very far from everyday care, and it is not a cure.
Source: PubMed, October 9, 2026 · Read the original
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