Stephen R. Hammes, M.D., Ph.D.

The Hammes laboratory studies steroid signaling and steroid production, with a focus on how steroids regulate fertility as well as how steroid promote hormone-sensitive cancer such as breast and prostate cancer.

With regard to steroid signaling, the Hammes laboratory pioneered research related to rapid, extranuclear, or "nongenomic," steroid effects, demonstrating that these rapid responses that initiate at or near the membrane of cells are critical for the subsequent steroid-mediated nuclear effects on transcription. The Hammes laboratory demonstrated that extranuclear androgen signaling via classical androgen receptors located outside of the nucleus initiate rapid activation of G protein and kinase signals that modulate normal fertility in males and females, as well as prostate cancer progression in response to androgens.

The Hammes laboratory was also one of the first to use genetic mouse models to demonstrate that androgen signaling in granulosa cells of the ovary (both nuclear and extranuclear effects) is critical for normal follicle development and subsequent ovulation. Too much androgen signaling, as seen in the disease polycystic ovary syndrome, leads to excessive and unregulated follicle growth.

The Hammes laboratory has also been studying androgen effects on prostate cancer, demonstrating that these same signaling extranuclear and nuclear pathways work together to regulate prostate cancer growth. The laboratory has also recently taken an interest in inflammation and its effects on prostate cancer progression.

Finally, the Hammes laboratory studies a rare lung disease found almost exclusively in women called lymphangioleiomyomatosis, or LAM. The laboratory has developed a mouse model for this disease, and is currently examining the roles of estrogen as well as inflammation in progression of this devastating disorder.