Julie Ostrander, PhD

Associate Professor of Medicine, Division of Hematology, Oncology and Transplantation

Julie Ostrander

Contact Info

Lab Phone 612-624-8201

Mailing Address:
Cancer and Cardiovascular Research Building
1st Floor Mailroom CCRB
2812A (Campus Delivery Code)
2231 6th St SE
Minneapolis, MN 55455

Administrative Phone

Administrative Email

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 Cellular Mechanisms of 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.


  • Growth factor signaling
  • Biomarkers of breast cancer progression
  • Therapy resistance
  • Breast cancer stem cells
  • PELP1

Professional Associations

  • Endocrine Society
  • American Association of Cancer Research (AACR)
  • Masonic Cancer Clinic
  • Cellular Mechanisms


Research Summary/Interests

Dr. Ostrander’s research focuses on studying the scaffolding protein PELP1 in the context of breast cancer progression. Our recent studies have found that PELP1 signaling 1) promotes cell survival in the presence of tamoxifen, 2) enhances breast epithelial cell migration through upregulation inflammatory cytokines and chemokines, and most recently 3) promotes CSC phenotypes in models of ER-positive breast cancer. We have identified a novel cytoplasmic interaction between PELP1 and SRC-3. The objective of our current research is to identify the molecular mechanisms associated with PELP1-induced BCSC phenotypes and therapy resistance.


  • Dwyer AR, Truong TH, Ostrander JH, Lange CA. 90 YEARS OF PROGESTERONE: Steroid receptors as MAPK signaling sensors in breast cancer: let the fates decide. J Mol Endocrinol. 2020 Jul;65(1):T35-T48. doi: 10.1530/JME-19-0274. PubMed PMID: 32209723; PubMed Central PMCID: PMC7329584.
  • Regan Anderson, TM, Ma S, Perez Kerkvliet, C, Peng, Y, Helle, TM, Krutilina, RI, Raj, GV, Cidlowski, JA, Ostrander, JH, Schwertfeger, KL, Seagroves, TN, Lange, C.A. Taxol induces brk-dependent prosurvival phenotypes in TNBC cells through an AhR/GR/HIF-driven signaling axis. MCR; 2018; 16(11); 1761–72.
  • Truong, TH, Lange, CA, Ostrander, JH. Targeting steroid receptor coactivators to inhibit breast cancer stem cells. Oncoscience. 201;5(11-12):281-282
  • Truong TH, Hu H, Temiz NA, Hagen KM, Girard BJ, Brady NB, Schwertfeger KL, Lange CA*, and Ostrander JH* Cancer Stem Cell Phenotypes in ER+ Breast Cancer Models Are Promoted by PELP1/AIB1 Complexes. Molecular cancer research. 2018;16(4):707-719. *Denotes co-principal investigators
  • Girard BJ, Knutson TP, Kuker B, McDowell K, Schwertfeger KL, Ostrander JH. Cytoplasmic Localization of Proline, Glutamic Acid, Leucine Rich Protein 1 (PELP1) Induces Breast Epithelial Cell Migration through Upregulation of Inhibitor of kappa B Kinase Epsilon and Inflammatory Crosstalk with Macrophages. J Biol Chem. 2017;292(1):339-350.
  • Leehy K, Regan-Anderson T, Knutson T, Raj G, Lange CA, and Ostrander JH. Post-translational Modifications to Glucocorticoid (GR) and Progesterone Receptors (PR): Context-Dependent Mediators of Cell Fate in Breast Cancer (review). J Mol Endocrinol. 2016;56(3):R99-R114.
  • 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;10(3):e0121206.
  • 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.
  • PELP1: A review of PELP1 interactions, signaling, and biology. Girard BJ, Daniel AR, Lange CA, Ostrander JH. Mol Cell Endocrinol. 2014;;382(1):642-651.