A protein drives Cushing's disease tumor growth, and an approved drug slowed it in mice
Original title: Phosphoproteomic dysregulation promotes tumor proliferation in Cushing's disease.
How far along is this research?
- Lab cells
- Animals
- Review
- Tested in people
This was done in animals, not people. Most findings at this stage never become treatments.
This was only done in cells and in mice, not in people.
The short version
A drug already approved for another illness slowed these tumor cells in mice.
What was studied. Pituitary tumors make up as much as 20% of tumors that start in the brain. Researchers compared pituitary tumors from people with Cushing's disease to normal pituitary tissue, then tested cells and mice.
What they found. Gene changes had switched a protein program back on that normally turns off after birth. The tumor cells made too much of a protein called PPP1R17. When normal mouse pituitary cells were made to produce extra PPP1R17, they grew fast like tumor cells. A drug called fingolimod reversed that fast growth in cells and in mice.
What this means, and what it doesn't
What it could mean: It points to a possible drug target for Cushing's disease. The drug tested is already approved for a different illness, so more testing could move faster.
What it doesn't mean: This does not mean fingolimod treats Cushing's disease in people. The work was done in cells and in mice only. No one has shown it helps a patient with this kind of tumor. It is not a cure, and it is not care you can ask a doctor for today.
Source: PubMed, September 29, 2026 · Read the original
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