Northwestern University Feinberg School of Medicine

Center for Genetic Medicine

Serdar E Bulun, MD

Serdar E Bulun, MD

Chair, Department of Obstetrics and Gynecology

John J. Sciarra Professor of Obstetrics and Gynecology

Professor of Obstetrics and Gynecology (Reproductive Science in Medicine)


Administrative office: 312-472-3980
Laboratory: 312-503-0524

Prentice Women's Hospital
250 East Superior Street
Suite 03-2306
Chicago IL 60611

sarah.cuneo( at )

Hospital Affiliations

I am on the medical staff at the following Feinberg-affiliated hospital(s)

Education and Certification

MD: Istanbul University (1983)
Residency: University of Arizona College of Medicine, Pathology (1987)
Internship: Columbia University College of Physicians and Surgeons, Obstetrics Gynecology (1988)
Residency: SUNY/State University of New York, Buffalo, Obstetrics Gynecology (1991)
Fellowship: Parkland Memorial Hospital (1993)
Board Certification: Obstetrics & Gynecology, Reproductive Endocrinology & Infertility


Description of Interests

The laboratory research of Serdar E. Bulun, MD, focuses on studying estrogen biosynthesis and metabolism, in particular aromatase expression, in hormone-dependent human diseases such as breast cancer, endometriosis and uterine fibroids. A team of investigators works on understanding the epitheial-stromal interactions and aromotase overexpression in breast cancer tissue. Since aromatase inhibitors treat breast tumors primarily via suppressing intratumoral estrogen biosynthesis, these efforts are important for discovering new targets of treatment. Another team studies endometriosis. Basic data from this laboratory led to the introduction of aromatase inhibitors into endometriosis treatment. Human tissues and a primate model are used to elucidate cellular and molecular mechanisms responsible for the development of endometriosis. Regulation of aromatase expression is also studied in uterine fibroids, benign tumors that are dependent on estrogen for growth, by a third team. A fourth team is investigating the link between progesterone action and estrogen inactivation in normal endometrium and endometriosis. Lastly, a fifth team has identified novel mutations that cause familial excessive estrogen formation syndrome. This syndrome is characterized by short stature, gynecomastia, and hypogandism in males and early breast development and irregular menses in females. In this syndrome, heterozygous inversions in chromosome 15q21, which cause the coding region of the aromatase gene to lie adjacent to constitutively active cryptic promoters that normally transcribe other genes, result in estrogen excess owing to the overexpression of aromatase in many tissues.

Interests (Keywords)

Breast Disease; Cancer Biology; Endocrinology; Infertility - Female; Sexual dysfunction; Women's Health; Women's Reproductive Health

Research and Publications

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