A new target may help when Hedgehog tumor drugs stop working
Original title: DYRK2 inhibition overcomes resistance to SMO inhibitors in Hedgehog-driven tumors.
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 only done in cells in a lab, not in people.
The short version
In lab cells, blocking a protein called DYRK2 shut down a tumor growth signal that current drugs could not stop.
What was studied. Some tumors grow because of a signal called Hedgehog. Drugs like vismodegib and sonidegib block that signal, but tumors can change and stop responding. Researchers used lab cells with one of these drug-resistant changes, then removed or blocked a protein called DYRK2.
What they found. Blocking DYRK2 turned down the Hedgehog growth signal in the resistant cells. Vismodegib did not stop these cells from forming growth clusters. Blocking DYRK2 did reduce that cluster growth in medulloblastoma cells.
What this means, and what it doesn't
What it could mean: Drug resistance is a real problem for people taking Hedgehog drugs today. This work points to a possible new way around it. Right now it gives scientists a target to keep studying.
What it doesn't mean: This was done in cells in a dish, not in people. No one knows yet if it is safe or helpful for patients. There is no DYRK2 drug a doctor can offer you. It is not a cure, and it is far from everyday care.
Source: PubMed, October 27, 2026 · Read the original
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