Two-Drug Combo Reverses Resistance in Prostate Cancer Study — SkimNews
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- University of Michigan researchers identified two pathways that can be simultaneously targeted to treat prostate tumors that have undergone transdifferentiation, publishing the work in JCI Insight.
- BET bromodomain inhibitors alone slowed prostate cancer cell growth but failed to kill cancer cells, prompting the team to seek a complementary drug class.
- DNMT inhibitors, already FDA-approved for blood cancer and other conditions, can reactivate glandular genes that are silenced when prostate cancer cells change identity.
- The two-drug combination reversed significant portions of gene expression changes in tumors and sharply reduced tumor growth in both cell lines and mouse models, even at doses far lower than the recommended level.
- Will Storck, a research lab specialist in the Alumkal lab, said the combination was well tolerated by mice and produced a significant reduction in tumor growth.
- Joshi Alumkal and the team plan to identify biomarkers predicting which patients would benefit and to develop clinical trials testing the combination in humans.
- The researchers believe the two-drug strategy could eventually extend to lung and pancreatic cancers, which also undergo transdifferentiation.
Why it matters: Prostate cancer is the second-leading cause of cancer death among U.S. men, and nearly all patients on androgen receptor inhibitors eventually develop resistance. The BET+DNMT combination offers a mechanism to attack tumors that have already escaped standard therapy, and Alumkal's team specifically frames prevention of transdifferentiation as key to patient survival — a clinical use case distinct from treating resistance after it appears.
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