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Getting the latest healthcare news for you
Getting the latest healthcare news for you
Some prostate cancers dodge treatment by literally changing what kind of cell they are — but researchers may have found a way to fight back. A University of Michigan team found that combining two drug classes reversed these cellular identity shifts and significantly slowed tumor growth in preclinical experiments. The approach could eventually apply to other hard-to-treat cancers too.
Some prostate cancers are remarkably crafty — when standard hormone-blocking treatments close in, they escape by changing their cellular identity entirely, a process called transdifferentiation. This makes them nearly impossible to treat with existing therapies. Now, University of Michigan researchers think they've found a way to outsmart this survival trick.
Publishing in JCI Insight, the team identified two biological pathways involved in this identity switch — one that activates alternative cell programs and another that silences glandular genes. They tested a combination of BET bromodomain inhibitors (which block the alternative identity programs) and DNMT inhibitors (which help restore lost glandular genes), finding the combo outperformed either drug alone in both cell lines and mouse models.
Key Takeaways:
Why it matters: Prostate cancer is the second leading cause of cancer death in American men, and resistance to androgen receptor inhibitors is nearly universal. This strategy could offer a new lifeline for patients with aggressive, treatment-resistant disease — and may have broader implications for other cancers, including lung and pancreatic, that use similar identity-shifting escape mechanisms.
