Dr. Hammes received his B.A. in chemistry from Cornell University in 1985, where he worked with Dr. Barbara Baird studying the IgE receptor. Dr. Hammes then entered the MD/PhD program at Duke. For his PhD, Dr. Hammes studied retroviral gene regulation with Dr. Warner Greene. He then traveled to San Francisco, where he completed an internship and residency in General Medicine, followed by a fellowship in Endocrinology. For his postdoctoral research, Dr. Hammes again chose an alternative direction, working with a cardiologist rather than an endocrinologist. He trained with Dr. Shaun Coughlin, where he studied G protein-coupled receptors.
In 1999, Dr. Hammes left UCSF to become faculty at the UT Southwestern Medical Center in Dallas, where he started an entirely new research program, choosing to study transcription-independent, or nongenomic, steroid signaling. Specifically, Dr. Hammes studies steroid-triggered maturation (meiotic progression) of oocytes, one of the few physiologically relevant steroid-triggered processes that is generally accepted to be nongenomic. Dr. Hammes has recently expanded his work to study ovarian development and function, with a focus on diseases of androgen excess such as polycystic ovarian syndrome.
Finally, in 2009 Dr. Hammes moved back to Upstate New York, where he is the Louis S. Wolk Professor of Biomedical Research and the Chief of the Division of Endocrinology at the University of Rochester Medical Center.
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 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.