PhD, University of North Carolina at Chapel Hill, Chapel Hill, NC
Julie Ostrander, Ph.D. is an Assistant Professor in the Department of Medicine at the University of Minnesota and a member of the Women’s Cancer Program at the University of Minnesota Masonic Cancer Center. Dr. Ostrander received her Ph.D. from the University of North Carolina at Chapel Hill. She holds memberships in the American Association for Cancer Research and the Endocrine Society.
- Biomarkers of breast cancer progression and response to chemoprevention
- Growth factor signaling
Research Summary/InterestsDr. Ostrander’s research interests focus on identifying biomarkers to identify pre-invasive breast cancer and response to chemoprevention. The objective of her current research is to identify the molecular mechanisms associated with PELP1-induced breast cancer initiation. PELP1 was first identified as an estrogen receptor (ER) co-activator in ER+ breast cancer cell lines. Subsequent studies found that PELP1 functions in ER+ and ER- breast cancer and is overexpressed in 80% of invasive breast cancers. While PELP1 is primarily localized to the nucleus in the normal breast epithelial cells, in about 40% of invasive breast tumors a significant amount of PELP1 is localized in the cytoplasm. Dr. Ostrander’s laboratory has found that altered localization of PELP1 to the cytoplasm promotes breast cancer initiation and cell survival in the presence of tamoxifen.
The focus of a separate project is to use endogenous fluorophores to determine whether differences exist in normal and high-risk breast tissues, as well as breast cancer tissue. The endogenous fluorophores NADH and FAD are two of the principal electron donors and acceptors in cellular metabolism, respectively. The optical redox ratio is a measure of cellular metabolism and can be determined by the ratio of NADH/FAD. We have found that the optical redox ratio is higher in breast cancer cell lines compared to normal mammary epithelial cells. Additionally, we observed a statistically significant increase in the optical redox ratio of ER(+) breast cancer cell lines. The overall goal of this research is to determine if endogenous fluorophors can detect high-risk, pre-invasive changes in normal breast tissue.
- Lofgren KA, Ostrander JH, Housa D, Hubbard GK, Locatelli A, Bliss RL, Schwertfeger KL, Lange CA. Mammary gland specific expression of Brk/PTK6 promotes delayed involution and tumor formation associated with activation of p38 MAPK. Breast Cancer Res. 2011 Sep 17;13(5):R89.
- Ostrander JH*, D’Amato NC*, Cardiff RD, Young LJ, Simin K, Bachelder RE, Ibarra-Drendall C, Bowie ML, Yu D, Delrow J, Dawson A, Yee LD, Mrózek K, Clay T, Osada T, Troch MM, Seewaldt VL. Phenotypic Plasticity in an Aggressive Triple-Negative Human Breast Cancer: Human biology is recapitulated by a novel model system. PLoS One. 2012;7(9) *Authors contributed equally to this manuscript.
- Girard BJ, Daniel AR, Lange CA, Ostrander JH. PELP1: A review of PELP1 interactions, signaling, and biology. Mol Cell Endocrinol. 2014 Jan 25;382(1):642-51.
- Daniel AR, Gaviglio AL, Knutson TP, Ostrander JH, Ravindranathan P, Peng Y, Raj GV, Yee D, Lange CA. Progesterone receptor-B enhances estrogen responsiveness of breast cancer cells via scaffolding PELP1- and estrogen receptor-containing transcription complexes. Oncogene. 2014 Jan 27. 24469035. PMCID: In progress
- Girard BJ, Regan-Anderson TM, Lem S, Nicely J, Seewaldt VL, Ostrander JH. Cytoplasmic PELP1 and estrogen-related receptor gamma protect human mammary epithelial cells from tamoxifen-induced cell death. PLoS One. 2015 Mar 19;10(3).