NIH-funded study suggests that testosterone suppresses brain tumor growth in males
Research news: An NIH-funded Cleveland Clinic study reports that androgen loss (including testosterone) accelerated glioblastoma growth in male preclinical models via hypothalamus-pituitary-adrenal (HPA) axis activation, inflammation, and an immunosuppressive brain microenvironment. In an observational SEER analysis of >1,300 men with glioblastoma, supplemental testosterone use for non-cancer reasons was associated with improved survival (38% lower risk of death). Authors note the human findings are non-causal and support prospective clinical trials.
Research news (not a regulatory approval) — May 6, 2026
An NIH-funded team at Cleveland Clinic reported evidence that androgens may limit glioblastoma progression in males. In male mouse models, androgen loss (e.g., reduced testosterone) accelerated tumor growth and was linked to local inflammation and activation of the hypothalamus-pituitary-adrenal (HPA) axis. The researchers described downstream increases in stress hormones and a “tightened security” response in the brain that reduced immune-cell access, creating an immunosuppressive environment in which tumors progressed more freely. Testosterone did not show the same effect in female mice.
To explore clinical relevance, the investigators analyzed existing human data from the NIH/NCI Surveillance, Epidemiology, and End Results (SEER) database, including more than 1,300 men with glioblastoma. Men who were receiving supplemental testosterone for reasons unrelated to cancer had a reported 38% lower risk of death than those not receiving supplementation.
The authors emphasized that the SEER finding is observational and does not establish causality, but they argue that the concordance between preclinical and population-level observations supports further investigation in prospective clinical trials. They also highlighted androgen deprivation as a potential factor to evaluate in future glioblastoma studies.
Reference: Lee J et al. Nature (2026). DOI: 10.1038/s41586-026-10451-5.