Oesterreich Lab

The main interest of Dr. Oesterreich’s laboratory is to further our understanding of hormone action in breast cancer, with the goal to use this knowledge for improved diagnosis and endocrine treatment of breast cancer patients. Specifically, her group studies how the estrogen receptor (ER) functions, how its activity is regulated by co-activator and co-repressor proteins, and if and how these mechanisms are perturbed in cancer cells. The lab is interested in novel concepts of ER action, such as its role in repression of gene transcription, and the involvement of higher order chromatin structure in hormone response. The Oesterreich lab aims to identify genetic markers such as polymorphisms, or epigenetic changes such as DNA methylation, which might be able to predict a patient’s response to endocrine therapy, which can be used to “personalize medicine”. All of these studies include many aspects of translational breast cancer research utilizing basic biochemistry, molecular and cell biology, cell lines, mouse models and clinical samples from retrospective cohort studies, and from clinical trials.

Oesterreich Research Group

https://mageewomens.org/investigator/steffi-oesterreich-phd/


 

Kai Ding
Graduate Student Researcher


Zheqi Li
Graduate Student Researcher


Steffi Oesterreich, PhD
Professor & Vice Chair for Precision and Translational Pharmacology


Sayali Onkar
Graduate Student Researcher


Matthew Sikora, PhD
Postdoctoral Associate


Nilgun Tasdemir, PhD
Research Instructor

Steffi Oesterreich, PhD

Pathiraja TN, Nayak S, Xi Y, Jiang S, Garee JP, Edwards DP, Lee AV, Chen J, Shea MJ, Santen RJ, Gannon F, Kangaspeska S Jelinek J, Issa JJ, Richer JK, Elias A, Mcllroy M, Young L, Davidson NE, Schiff R, Li W, and Oesterreich S. Epigenetic reprogramming of HOXC10 in endocrine-resistant breast cancer. Science Transl med 6:229, 2014. PMID: 24670685.
Sikora Mj, Cooper KL, Bahreini A, Luthra S, Wang G, Chandran UR, Davidson NE, Dabbs DJ, Welm AL, Oesterreich S. Invasive lobular carcinoma cell lines are characterized by unique estrogen-mediated gene expression patterns and altered tamoxifen response. Cancer Res 74:1463-1472, 2014.  PMID: 24425047. PMCID: PMC3955299 [Available 2015/3/1]
Oesterreich S, Davidson NE. The search for ESR1 mutations in breast cancer. Nat Genet 45:1415-1416, 2013. PMID: 24270445
Oesterreich S, Brufsky AM, Davidson NE. Using mice to treat (wo)men: Mining genetic changes in patient xenografts to attack breast cancer. Cell Rep 4:1061-1062, 2013. PMID: 24075202
Oesterreich S, R Edwards and A Vlad.  Progestins:  Pro-senescence therapy for ovarian cancer:  Cell Cycle 12:1662-1663, 2013.
Hartmaier RJ, AS Richter, RM Gillihan, JZ Sallit, SE McGuire, J Wang, AV Lee, CK Osborne, BW O'Malley, PH Brown, J Xu, TC Skaar, S Philips, JM Rae, F Azzouz, L Li, J Hayden, NL Henry, AT Nguyen, V Stearns, DF Hayes, DA Flockhart and S Oesterreich.  A SNP in steroid receptor coactivator-1 disrupts a GSK3 beta phosphorylation site and is associated with altered Tamoxifen response in bone.  Mol Endo 26:220-227, 2012.
Watters RJ, PV Benos and S Oesterreich.  To bind or not to bind:  FoxA1 determines estrogen receptor action in breast cancer progression.  Breast Cancer Res 14:312, 2012.
Smith CL, I Migliaccio, V Chaubal, MF Wu, MC Pace, R Hartmaier, S Jiang, DP Edwards, MC Gutierrez, SG Hilsenbeck and S Oesterreich.  Elevated expression of the SMRT corepressor in breast cancer is associated with earlier tumor recurrence.  Breast Cancer Res Treat 136:253-265, 2012.
Steinman RA, AM Brufsky and S Oesterreich.  Zoledronic acid effectiveness against breast cancer metastases:  A role for estrogen in the microenvironment?  Breast Cancer Res 14:213, 2012.
Pathiraja TN, PB Shetty, J Jelinek, R He, R Hartmaier, AL Margossian, SG Hilsenbeck, JP Issa and S Oesterreich.  Progesterone receptor isoform-specific promoter methylation:  Association of PRA methylation with worse outcome in breast cancer patients.  Clin Cancer Res 17:4177-4186, 2011.
Garee JP, R Meyer and S Oesterreich.  Co-repressor activity of scaffold attachment factor B1 requires sumoylation.  Biochem Biophys Res Commun 408:516-522, 2011.
Oesterreich S, AV Lee and NE Davidson.  Is it time to reSET the standard for estrogen receptor testing in breast cancer?  J Clin Oncol 28:4101-4103, 2010.

Nilgun Tasdemir, PhD

Bossart EA‡, Tasdemir N‡, Sikora MJ, Bahreini A, Levine KM, Chen J, Basudan A, Jacobsen BM, Burns TF, Oesterreich S. (2019). SNAIL is induced by Tamoxifen and leads to growth inhibition in invasive lobular breast carcinoma. Breast Cancer Res Treat. doi: 10.1007/s10549-019-05161-8. [Epub ahead of print]. ( equal contributors).
 
Tasdemir N, Bossart EA, Li Z, Zhu L, Levine KM, Jacobsen BM, Tseng GC, Davidson NE, Oesterreich S. (2018). Comprehensive phenotypic characterization of human invasive lobular carcinoma cell lines in 2D and 3D cultures. Cancer Research. 8(21):6209-6222.
 
Banito A, Li X, Laport A, Roe JS, Sánchez-Vega F, Huang CH, Dancsok A, Hatzi A, Chen CC, Tschaharganeh DF, Tasdemir N, et al. (2018). The SS18-SSX oncoprotein hijacks KDM2B-PRC1.1 to drive synovial sarcoma. Cancer Cell. 33(3): 527-541.
 
Sakamaki J, Wilkinson S, Hahn M, Richter B, Tasdemir N, J O’Prey, et al. (2017). Bromodomain protein BRD4 is a transcriptional repressor of autophagy and lysosomal function. Molecular Cell. 66(4): 517-532.
 
Tasdemir N, Banito A, Roe JS, Alonso-Curbelo D, Camiolo M, Tschaharganeh DF, Huang CH, Aksoy O, Bolden JE, Chen CC, Fennell M, Thapar V, Chicas A, Vakoc CR, Lowe SW. (2016). BRD4 connects enhancer remodeling to senescence immune surveillance. Cancer Discovery. 6(6): 612-629.
 
Cheloufi S, Elling U, Hopfgartner B, Jung YL, Murn J, Ninova M, Hubmann M, Badeaux AI, Euong Ang C, Tenen D, Wesche DJ, Abazova N, Hogue M, Tasdemir N, et al. (2015). The histone chaperone CAF-1 safeguards somatic cell identity. Nature. 528: 218-224.
 
Bolden JE‡, Tasdemir N‡, Dow LE‡, van Es JH, Wilkinson JE, Zhao Z, Clevers H, Lowe SW. (2014). Inducible in vivo silencing of Brd4 identifies potential toxicities of sustained BET protein inhibition. Cell Reports. 8(6): 1919-29. (equal contributors).