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Christy R. Hagan, Ph.D.

Assistant Professor
Biochemistry and Molecular Biology

Colorado College, Colorado Springs, CO, B.A. in Biochemistry, cum laude, 1998
Human Gene Therapy Research Institute, Des Moines, IA, Pre-Doctoral Fellow, 1998 - 2000
University of Chicago, Chicago IL, PH.D. in Cancer Biology, 2006
Northwestern University, Postdoctoral Fellowship, 2006 – 2008
University of Minnesota, Postdoctoral Fellowship, 2008-2014
University of Kansas Medical Center, Kansas City, KS, Assistant Professor, 2015 – present

Interests: Role of hormones in breast cancer, crosstalk beween the immune system and steroid receptor action

Publications: Click here

913-588-0795
chagan@kumc.edu
Office:  1063 Hemenway
Lab:  1022 Hemenway

My lab studies the role of hormones in breast cancer. In particular, we are interested in how the ovarian steroid hormone, progesterone, works together with its receptor, the progesterone receptor (PR), to influence breast cancer biology. Mounting clinical data continues to implicate progesterone and PR in breast cancer progression. Upon diagnosis, nearly 70% of breast cancers express PR and the estrogen receptor (ER). In contrast, only 7-10% of normal luminal epithelial cells express ER and PR. ER action in breast cancer has been well studied and as a result, ER has proven to be an excellent target for current endocrine-based therapies. However, despite convincing clinical trial data implicating progesterone in the development of invasive breast cancer, the role of progesterone/PR in breast cancer has been largely understudied. Despite maintaining receptor (ER/PR) expression, many breast cancer patients eventually progress to hormone-independence, failing current (largely ER/estrogen based) endocrine therapies. Therefore, ER-independent functions of PR are of great clinical interest.

Our current work is focused on how PR may promote breast tumor progression through evasion of immune surveillance. Interferon-activation is a key step in immune surveillance and destruction of nascent tumors. We recently described how interferon-stimulated genes, an end product of interferon signaling, are transcriptionally repressed by PR through modulation of STAT1 and STAT2. This represents a novel subset of genes not previously known to be regulated by PR. Moreover, PR-dependent attenuation of interferon signaling suggests a mechanism through which PR may aid early breast cancer lesions in escaping immune surveillance. As such, we have shown that PR promotes immunosuppressive changes in the immune microenvironment of the mammary gland. We've shown that these immunosuppressive changes lead to the development of mammary gland tumors. These data have significant implications for the use of progesterone-containing hormone replacement therapy in post-menopausal women, as well as underscore the importance of studying anti-progestins (synthetic progesterone) as novel chemo-preventative agents for breast cancer. Moreover, modulating PR action in breast tumors may make these tumors more susceptible to treatment with new immunotherapy agents, such as checkpoint inhibitors.

Hagan Lab 2020



Last modified: Feb 04, 2020

Contact

Christy R. Hagan, Ph.D.
Assistant Professor

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