Weizmann scientists show how many prostate tumours escape hormone therapy

A team led by Prof. Yosef Yarden of the Weizmann Institute of Science reported in May 2026 why many prostate cancers stop responding to hormone therapy, the standard treatment for advanced disease. The study, published in EMBO Molecular Medicine with collaborators including the US National Cancer Institute, was carried out largely by Dr. Arunachalam Sekar in Yarden's laboratory.

Prostate tumours usually depend on male hormones, or androgens, so doctors lower androgen levels or block their receptor. Many tumours eventually adapt and the cancer returns. The Weizmann group focused on a gene fusion, in which two genes break and join into one hybrid, that is present in roughly half of all prostate cancers. They found that the protein made by this fused gene teams up with the receptor for cortisol, the body's main stress hormone, and switches on growth genes. When androgen signalling is shut down by therapy, this cortisol route takes over and keeps the tumour growing.

In mice, treating tumours with both an androgen blocker and a drug that blocks the cortisol receptor slowed growth and extended survival more than either treatment alone. One of the drugs that worked in the mice is a cortisol-receptor blocker that the US Food and Drug Administration recently approved for ovarian cancer, which could make it quicker to test in men. The researchers checked patient biopsy samples to confirm how common the fusion is, but the treatment results so far come only from animal models.

The findings also carry a caution for current practice. Steroid drugs such as prednisone are often given to men with advanced prostate cancer, and the study suggests they could, in principle, feed tumours that carry the fusion. The authors propose that patients be tested for the fusion so that those at higher risk of resistance can be identified and treated differently.