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

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The Hammes laboratory studies how steroidogenesis and steroid signaling in the ovary regulate ovarian development and function.

First, they use frog and mouse models of steroid-triggered oocyte maturation (meiotic resumption) to study transcription-independent, or nongenomic, steroid signaling. The laboratory has made many important discoveries regarding the roles of androgens, androgen receptors, and G proteins in regulating the maturation process. They are interested in studying how this nongenomic androgen signaling might affect ovarian development and function in diseases of androgen excess, such as polycystic ovarian syndrome (PCOS).

Second, the laboratory uses using mouse models to characterize the intracellular signaling pathways triggered by gonadotropins during steroidogenesis, focusing on potential signaling molecules that can be specifically targeted to reduce ovarian androgen production in PCOS.

Third, the laboratory is interested in understanding ovarian follicle development, and is studying a novel GATA-like protein that is expressed in granulosa cells, may regulate steroidogenesis, and is essential for normal embryonic follicle development and germ cell survival.

Finally, the laboratory has recently begun to study how transcription-independent androgen signaling can regulate steroid-sensitive tumors, such as prostate cancer. This work involves characterization of the mechanisms regulating steroid-triggered MAPK signaling, focusing on potential therapeutic targets that can be translated into the clinic.

Current Appointments

• Chief - Department of Medicine (SMD)
• Louis S. Wolk Distinguished Professorship in Medicine - Department of Medicine (SMD)
• Professor - Department of Medicine (SMD)
• Professor - Department of Pharmacology and Physiology (SMD)

Lab Description

The Hammes lab studies how steroidogenesis and steroid signaling in the ovary regulate ovarian development and function, focusing on potential targets to reduce androgen production/signaling in PCOS.