420 Washington Ave SE
420 Washington Ave SE
Minneapolis, MN 55455
My laboratory research is focused in the areas of cancer stem cells (CSCs), therapy resistance, steroid receptors (SRs), and cancer metabolism. Our research aims to define the molecular links between oncogenic signaling and altered metabolic events in breast cancer progression and metastasis that contribute to endocrine and chemotherapy resistance.
Late recurrence of metastatic disease stemming from acquired therapy resistance remains a significant health burden for women with ER+ breast cancer. Contributing factors include breast cancer stem cells (CSCs) which are poorly proliferative and frequently exist as a minority population in recurrent therapy resistant tumors.
Our current objectives are centered on defining how steroid receptors (SRs) (e.g., estrogen receptor [ER], progesterone receptor [PR]) and their associated co-activators mediate the survival and expansion of therapy resistant breast CSCs with emphasis on oncogenic signaling pathways and metabolic reprogramming. Identifying and targeting reversible events that drive metastatic ER+ breast tumor cells is an unmet need that has the potential to extend patient lives and improve well-being.
Our laboratory employs a wide variety of techniques to investigate the CSC population at the gene and protein level. We also use a variety of in vitro (breast cancer cell lines), pre-clinical (patient-derived organoids, PDxO), and in vivo (xenograft) models to achieve our research goals. Our research interests broadly include cancer stem cells, signal transduction, gene regulation, cancer metabolism, post-translational modifications, therapy resistance, breast cancer, and cancer biology
- Truong, T.H., Benner, B., Hagen, K.M., Temiz, N.A., Perez Kerkvliet, C., Wang, Y., Cortes-Sanchez, E., Yang, C.-H., Trousdell, M.C., Pengo, T., Guillen, K.P., Welm, B.E., Dos Santos, C.O., Telang, S., Lange, C.A., and Ostrander, J.H. (2021). “PELP1/SRC-3 dependent regulation of metabolic kinases drives therapy resistant ER+ breast cancer.” Oncogene. 40(25): 4384-4397.
- Truong, T.H.*, Dwyer, A.R.*, Diep, C., Hu, H., Hagen, K.M., and Lange, C.A. (2019). “Phosphorylated progesterone receptor isoforms mediate opposing stem-like and proliferative breast cancer cell fates.” Endocrinology. 160(2), 430-446. *Equal contribution
- Truong, T.H., Hu, H., Temiz, N.A., Hagen, K.M., Girard, B.J., Brady, N.J., Schwertfeger, K.L., Lange, C.A., and Ostrander, J.H. (2018). “Cancer Stem Cell Phenotypes in ER+ Breast Cancer Models Are Promoted by PELP1/AIB1 Complexes.” Mol. Cancer Res. 16 (4) 707-719.
- Truong, T.H., Ung, P.M., Palde, P.B., Paulsen, C.E., Schlessinger, A., and Carroll, K.S. (2016). “Molecular Basis for Redox Activation of Epidermal Growth Factor Receptor Kinase.” Cell Chem. Biol. 23 (7), 837-848.
- Paulsen, C.E., Truong, T.H., Garcia, F.J., Homann, A., Gupta V., Leonard, S.E., Carroll, K.S. (2011). “Peroxide-dependent sulfenylation of the EGFR catalytic site enhances kinase activity.” Nat. Chem. Biol. 8 (1), 57-64.
Education and background
- Postdoctoral Fellow - University of Minnesota Masonic Cancer Center
- Ph.D. in Chemistry (Chemical Biology) - University of Michigan, 2014
- B.S. in Chemistry - Texas A&M University, 2008
- NIH/NCI K22 Transition Career Development Award, 2023
- METAvivor Early Career Investigator Award, 2020
- NIH/NCI F32 Ruth L. Kirschstein Postdoctoral Individual National Research Service Award (NRSA), 2017