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

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

Medicine — Endocrine/Metabolic — Endocrinology, Diabetes and Metabolism

Accepting New Patients

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

Medicine — Endocrine/Metabolic — Endocrinology, Diabetes and Metabolism

Accepting New Patients


Locations

University of Rochester Medical Center
School of Medicine and Dentistry
601 Elmwood Ave, Box 693
Rochester, NY 14642
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phone

Appointments

(585) 275-8762

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Fax

(585) 273-1288

About Me

Credentials

Education:

MD, PhD | Duke University School of Medicine — 1992

Post-doctoral Training & Residency:

Fellowship in Endocrinology at University of California, San Francisco Medical Center — 1995 - 1999
Research in at Duke University Medical Center — 1993 - 1993
Internship in Internal Medicine at University of California, San Francisco Medical Center — 1993 - 1994
Residency in Internal Medicine at University of California, San Francisco Medical Center — 1994 - 1995

Research

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.

Publications:

Ma X, Hayes E, Biswas A, Seger C, Prizant H, Hammes SR, Sen A. "Androgens Regulate Ovarian Gene Expression Through Modulation of Ezh2 Expression and Activity." Endocrinology.. 2017 Sep 1; 158(9):2944-2954.

Lerman I, Garcia-Hernandez ML, Rangel-Moreno J, Chiriboga L, Pan C, Nastiuk KL, Krolewski JJ, Sen A, Hammes SR. "Infiltrating Myeloid Cells Exert Protumorigenic Actions via Neutrophil Elastase." Molecular cancer research : MCR.. 2017 Sep 0; 15(9):1138-1152. Epub 2017 May 16.

Miedlich SU, Taya M, Young MR, Hammes SR. "Paxillin and embryonic PolyAdenylation Binding Protein (ePABP) engage to regulate androgen-dependent Xenopus laevis oocyte maturation - A model of kinase-dependent regulation of protein expression." Molecular and cellular endocrinology.. 2017 Jun 15; 448:87-97. Epub 2017 Mar 28.

View All Publications

Links:

Lab Website