Lab-grown blood vessels point to a protein behind VHL syndrome
Original title: HNRNPC-mediated RNA processing promotes VHL-associated excessive vasculogenesis in von Hippel-Lindau syndrome revealed from patient-derived blood vessel models
How far along is this research?
This is a preprint. Other scientists have not checked it yet, so treat it as an early signal rather than an answer.
This was done with cells in a lab and in animals, not in people.
The short version
Scientists grew blood vessel cells from patients to learn why too many vessels form in von Hippel-Lindau syndrome.
What was studied. Researchers made stem cells from people with von Hippel-Lindau syndrome, an inherited condition that causes too many blood vessels, tumors, and cysts. They turned those stem cells into blood vessel cells and compared them with cells from healthy donors. They also edited the VHL gene in cells to match.
What they found. The patient cells grew too many blood vessels. When placed in animals, they formed lesions packed with vessels and odd cell growth. A protein called HNRNPC built up in the patient cells. That build up turned out to be key to the extra vessel growth, and it worked apart from the protein that today's drugs target.
What this means, and what it doesn't
What it could mean: HNRNPC could become a new target for future drugs. Drugs now approved for this syndrome aim at a different protein, and they do not help enough for many people with kidney cancer. A new target gives researchers another path to try. The lab model itself also gives them a better way to study the disease.
What it doesn't mean: This does not mean a new treatment is coming soon. The work was done with cells in a dish and in animals. No drug for HNRNPC was given to a person in this study. Nothing here is a treatment you can ask your doctor for, and it is not a cure. Many ideas that work in the lab never work in people.
Source: bioRxiv (preprint), November 2, 2026 · Read the original
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