1. Personal Statement

I am a physician-scientist and breast medical oncologist studying mechanisms of tumor initiation and progression. My laboratory helped identify glucocorticoid receptor (GR) signaling as a pathway involved in solid tumor progression, mainly through a cell autonomous process related to cell survival and proliferation pathways downstream of GR activation. These findings have  led to clinical trials examining antagonism of GR–mediated tumor cell survival pathways in breast, ovarian, pancreatic and prostate cancer. Until 2019, as a tenured professor at The University of Chicago, I was Program co-Director for Basic Sciences in the UChicago Comprehensive Cancer Center. I moved to the University of Texas Southwestern (UTSW) to continue nuclear receptor studies in cancer with the goal to better understanding tumor cell GR in the context of the immune tumor microenvironment, which also expresses multiple cell types that are sensitive to glucocorticoids. My laboratory uses both animal modeling and molecular approaches to study GR signaling contributing to the development and progression of cancer. Our team was also the first to bring GR antagonism to clinical trials, in collaboration with colleagues Drs. Nanda/Fleming (breast/ovarian) and Szmulewitz (prostate cancer).  A recent Phase III trial in ovarian cancer that was based on our laboratory’s pre-clinical work found that treatment with a GR antagonist (a.k.a. GR modulator) and nab-paclitaxel is superior to nab-paclitaxel treatment alone platinum-resistant  HGSOC, resulting in longer time to recurrence and increased overall survival for the GR modulator treated group.

Selected ongoing and completed research projects that I would like to highlight include:

Selected Ongoing Research Support

R01 CA238519

Conzen (PI)

03/01/21-02/28/26

Estrogen and Glucocorticoid Receptor Crosstalk in ER+ Breast Cancer

R01 CA239719                                                                                                          

Conzen, Brady, McClintock (multi-PIs)                                              

07/01/20-07/30/26

Effects of Chronic Pubertal Stressors on Mammary Gland Biology and Cancer Risk

RR1900037

Conzen (PI)

06/01/19-05/31/26

Nomination of Suzanne D. Conzen, M.D. for a CPRIT Recruitment of Establish Investigators Award

Completed Research Support

R21 CA223426                                                                                                           

Conzen (PI)                                                                                             

06/16/2020-12/31/22

Identification of a Prognostic and Predictive Glucocorticoid Receptor Signature for Ovarian Cancer

R21 CA239048                                                                                                          

Conzen (PI)                                                                                           

06/16/2020-02//28/2022

NNMT Regulation of m6A RNA Modification in TNBC Progression

U01 CA195564                                                                                                          

Giger (PI), Role: Co-Investigator      

04/15/15-03/31/20

Quantitative Image Analysis for Assessing Response to Breast Cancer Therapy

P50 CA180995

Catalona (PI), Role: Co-Investigator      

08/18/15-07/31/20

SPORE in Prostate Cancer - Northwestern University

2. Positions, Scientific Appointments and Honors

Professional Experience

2019-present  Professor (with tenure) and Chief, Division of Hematology/Oncology, Department of Internal Medicine, University of Texas Southwestern Medical School, Dallas, TX.

                        Professor Emerita, The University of Chicago, Chicago, IL.

2010-2019       Professor (with tenure), Department of Medicine, Section of Hematology/Oncology, and the Ben             May Department of Cancer Biology, University of Chicago, Chicago, IL.

2006-2010       Secondary Appointment, Associate Professor, The Ben May Department for Cancer Research,   The University of Chicago, Chicago, IL (effective July 1, 2006).

2005-2009       Associate Professor, Department of Medicine, Section of Hematology/Oncology, University of     Chicago, Chicago, IL (effective July 1, 2005).

1. 2005. Assistant Professor, Department of Medicine, Section of Hematology/Oncology, University of      Chicago, Chicago, IL (effective July 1, 1998).

1996-1998       Post-Doctoral Fellow, Ben May Institute for Cancer Research, Senior Fellow, Section of   Hematology/Oncology, University of Chicago, Chicago, IL

1993-1996       Howard Hughes Medical Institute Physician Research Fellow, Department of Biochemistry,         Dartmouth Medical School, Hanover, NH

1990-1993       Hematology/Oncology Clinical Fellow, Dartmouth-Hitchcock Medical Center, Lebanon, NH

1987-1990       Intern and Resident, Department of Internal Medicine, New York Hospital-Cornell Medical           Center, Cornell University Medical College, New York NY

Honors

2020                Inductee, Association of American Physicians

2014-2019       Castle Connolly Top Doctors Award

2013                The University of Chicago Pritzker School of Medicine Arnold Mentorship Award

2015-2018       Senior Editor, Cancer Research

2011                Reviewer, Cancer Prevention Research Institute of Texas (CPRIT)

2010                Ad Hoc DOD-Integration Panel Member, Pre-doctoral and post-doctoral applications

2010                Triple-Negative Breast Cancer SEP, NIH, Member

2007                DOD-Breast Cancer Program  Synergistic Idea Award Review Panel

2006-2007       Track Leader, Tumor Biology, American Society of Clinical Oncology Program Committee

2006-2008       Chair, NIH “Cancer Etiology” (CE) Study Section

2006                Inductee, American Society of Clinical Investigation

2005-2019       Program Leader, Program 1 - Cell Signaling and Gene Regulation,

                        The University of Chicago Cancer Research Center

2004-2008       Permanent Member, NIH “Cancer Etiology” (CE) Study Section

2003                Susan Komen Foundation Molecular Biology Grant Review Panel

2001-2004       Fellow, Schweppe Foundation

2000-2012       Y-Me Medical Board Member

1. 2003. USDOD Breast Cancer Program Molecular Genetics Study Section Panel Member

1999-2000       Cancer Research Foundation Young Investigator award

3. Contributions to Science

1. Molecular mechanisms of GR signaling in breast cancer. Our laboratory uncovered a cell survival role for glucocorticoid receptor (GR) activity in triple-negative breast cancer (TNBC) progression and anti-apoptotic signaling in ER-negative breast, high-grade serous ovarian, and castrate-resistant prostate cancer models. GR activation results in the transcriptional activation of several important anti-apoptotic genes. Recently, in ER+ breast cancer we demonstrated that GR inhibits ER transcriptional activity through coordinated chromatin complex competition between ER and GR. These discoveries were reported in first author papers by trainees: Medical students*, postdoctoral fellows^#, graduate students^##, undergraduates^.

1. Wu W^#, Chaudhuri S^, Brickley DR, Pang D*, Karrison T, Conzen SD. Microarray analysis reveals glucocorticoid-regulated survival genes that are associated with inhibition of apoptosis in breast epithelial cells. Cancer Res 64:1757-64, 2004.
2. Pan D^#, Kocherginsky M, Conzen SD. Activation of the glucocorticoid receptor is associated with poor prognosis in estrogen-receptor-negative breast cancer. Cancer Res 71:6360-70, 2011.  PMC3514452.
3.    West DC^#, Pan D^#, Tonsing-Carter EY^#, Hernandez KM, Pierce CF^, Styke SC, Bowie KR, Garcia TI, Kocherginsky M, Conzen SD. GR and ER co-activation alters the expression of differentiation genes and associates with improved ER+ breast cancer outcome.  Mol Cancer Res. 2016 Aug;14(8):707-19. doi: 10.1158/1541-7786.
4. Porter BA^#, Frerich C^#, Lainé M, Clark AB*, Durdana I, Lee J, Taya M^#, Sahoo S, Greene GL, Bennett L, Conzen SD. Glucocorticoid Receptor Activation in Lobular Breast Cancer Is Associated with Reduced Cell Proliferation and Promotion of Metastases. Cancers (Basel). 2023 Sep 22;15(19):4679. doi: 10.3390/cancers15194679. PMID: 37835373; PMCID: PMC10571671.

2. GR modulation in castrate-resistant prostate cancer. In translational studies we were the first group to identify GR activation in prostate cancer cells following androgen signaling inhibition. We went on to develop models and clinical trials demonstrating that GR activation following androgen deprivation is associated with activation of several downstream, GR-mediated pro-oncogenic pathways.

1. Szmulewitz RZ^# , Chung E^# , Al-Ahmadie H, Daniel S, Kocherginsky M, Razmaria A, Zagaja GP, Brendler CB, Stadler WM, Conzen SD. Serum/glucocorticoid-regulated kinase 1 expression in primary human prostate cancers. Prostate 2012, Feb 1;72(2):157-64. doi:10.1002/pros.21416. PMCD PMC6000822.
2. Isikbay M*, Otto K, Kregel S, Kach J^#, Cai Y, Vander Griend DJ, Conzen SD, Szmulewitz RZ. Glucocorticoid receptor activity contributes to resistance to androgen-targeted therapy in prostate cancer. Horm Cancer 5:72-89, 2014. PMC4440041
3. Kach J^# , Long TM^# , Selman P, Tonsing-Carter EY, Bacalao MA, Lastra RR, de Wet L, Comiskey S, Gillard M^# , VanOpstall C, West DC^#, Chan WC, Griend DV, Conzen SD, Szmulewitz RZ. Selective Glucocorticoid Receptor Modulators (SGRMs) Delay Castrate-Resistant Prostate Cancer Growth. Mol Cancer Ther.2017 Aug;16(8):1680-1692. doi: 10.1158/1535-7163.MCT-16-0923. PMCID PMC5544558.
4. Bennett L, Jaiswal PK^#, Harkless RV, Long TM^#, Gao N, Vandenburg B, Selman P, Durdana I, Lastra RR, Vander Griend D, Adelaiye-Ogala R, Szmulewitz RZ, Conzen SD. Glucocorticoid receptor (GR) activation is associated with increased cAMP/PKA signaling in castrate-resistant prostate cancer. Mol Cancer Ther. 2023 Nov30. doi: 10.1158/1535-7163.MCT-22-0479. PMID: 38030378.

3. The role of psychosocial stressors and ensuing stress reactivity in rodent models of triple-negative breast cancer. We use our validated models of chronic social isolation as a psychosocial stressor to recapitulate high continuous stress exposure and dysregulated circulating glucocorticoids in vivo. These studies have revealed the tissue specific molecular roles of GR activation in vivo in breast cancer progression and susceptibility.

1. Luca F^#, Kashyap S, Southard C, Zou M^#, Witonsky D, Di Rienzo A, Conzen SD. Adaptive variation regulates the expression of the human SGK1 gene in response to stress. PLoS Genet. 5:e1000489, 2009. PMC2679193
2. Williams JB, Pang D^#, Delgado B, Kocherginsky M, Tretiakova M, Krausz T, Pan D^#, He J, McClintock MK, Conzen SD. A model of gene-environment interaction reveals altered mammary gland gene expression and increased tumor growth following social isolation. Cancer Prev Res (Phila) 2:850-61, 2009. PMC4707045
3. Volden PA^##, Skor MN, Johnson MB, Singh P^#, Patel FN, McClintock MK, Brady MJ, Conzen SD. Mammary adipose tissue-derived lysophospholipids promote estrogen receptor-negative mammary epithelial cell proliferation. Cancer Prev Res (Phila). 2016 Feb 9. pii: canprevres.0107.2015
4. Johnson MB^##, Hoffmann JN, You HM, Lastra RR, Fernandez S^##, Strober JW, Allaw AB, Brady MJ, Conzen SD, McClintock MK. Psychosocial Stress Exposure Disrupts Mammary Gland Development. J Mammary Gland Biol Neoplasia. 2018 Jun;23(1-2):59-73. doi: 10.1007/s10911-018-9392-4. Epub 2018 Apr 23. PMID: 29687293; PMCID: PMC6207373.

4. Developing models for understanding epitheial ovarian cancer therapy-resistance. Collaboration with ovarian cancer pathologist, gynecological oncologists and cancer modeling statisticians (Mayo Clinic) have lead to an intence interest in studying why epithelial ovarian cancer is so chemotherapy and immunotherapy resistant, and the role that the peritoneal microenvironment plays in this resistance.

1. Melhem A, Yamada SD, Fleming GF, Delgado B, Brickley DR, Wu W, Kocherginsky M, Conzen SD.Administration of glucocorticoids to ovarian cancer patients is associated with expression of the anti-apoptotic genes SGK1 and MKP1/DUSP1 in ovarian tissues. Clin Cancer Res. 2009 PMID: 19383827; 
2. Stringer-Reasor EM, Baker GM, Skor MN, Kocherginsky M, Lengyel E, Fleming GF, Conzen SD. Glucocorticoid receptor activation inhibits chemotherapy-induced cell death in high-grade serous ovarian carcinoma. Gynecol Oncol. 2015 Sep;138(3):656-62. PMC4556542.
3. Veneris JT, Darcy KM, Mhawech-Fauceglia P, Tian C, Lengyel E, Lastra RR, Pejovic T, Conzen SD, Fleming GF. High glucocorticoid receptor expression predicts short progression-free survival in ovarian cancer. Gynecol Oncol. 2017 Jul;146(1):153-160. PMC5955699.
4. Taya M, LeBlanc E, Bennett L, Conzen SD. Ovarian tumor-cell glucocorticoid receptor activity modulates cytokine secretion promoting recruitment and activation of immunosuppressive cells into the tumor microenvironment. J Endocr Soc. 2023 Oct 5; PMC10554397.

Complete List of Published Work in MyBibliography: 

https://www.ncbi.nlm.nih.gov/myncbi/suzanne.conzen.2/bibliography/public/