405-271-8001 ext. 32276
Dr. Wellberg's overall research goals include 1) identifying host (environment)-specific drivers of breast cancer therapy resistance in the context of obesity; 2) determining the effects of endocrine therapy on adipose, liver, and skeletal muscle biology, and 3) identifying and modeling the patient population at risk for adverse effects associated with endocrine therapy and implement appropriate ways to monitor and intervene to prevent breast cancer relapse. She combines basic research techniques, including culture of established and primary breast cancer cell lines, with preclinical (mouse and rat) models of obesity and clinical studies to comprehensively investigate the relationship between obesity, metabolic disease, and breast cancer progression.
Education:
- BS - Texas A&M University, College Station, TX; Biomedical Sciences (2004)
- PhD - Texas A&M University, College Station, TX; Toxicology (2009)
Fellowship:
- Research Instructor, Department of Pathology, Center for Women's Health Research, University of Colorado Denver (2014-2017)
- Post-doctoral Fellow, Department of Pathology, University of Colorado Denver (2009-2014)
Clinical/Research Interests:
Dr. Wellberg's training is in normal mammary gland biology and breast cancer metabolism. She currently holds an NCI R01 focused on FGF-FGFR signaling in endocrine-resistant breast cancer. Her lab studies the “vicious cycle” surrounding obesity and estrogen receptor positive (ER+) breast cancer. Dr. Wellberg's research focuses on the mechanisms through which obesity promotes breast cancer recurrence and progression, and also on the metabolic effects of estrogen deprivation that occur with endocrine (anti-estrogen) therapy. She has established a transplant-competent murine model of obesity and glucose intolerance, in which she grows breast cancer patient derived xenograft tumors (PDX) as well as established human breast cancer cell lines and she is currently investigating the mechanisms through which growth factor signaling initiates ligand-independent activation of the ER. Other projects in her laboratory focus on the excess risk for type 2 diabetes in breast cancer survivors, studying how obesity moderates the effects of ER antagonists and estrogen deprivation on adipose tissue expansion and adipocyte progenitor cell renewal and differentiation.
Funding:
- NIH R01CA241156 7/1/2019-6/30/2024: Growth factor signaling in obesity associated ER-positive breast cancer. Role: PI
- NIH R01CA251600 06/01/2020–05/31/2025: Disrupting Insulin Receptor Function in Breast Cancer. Role: Co-Inv
- DOD BCRP W81XWH2210042 09/01/2022–08/31/2025: Mechanisms of Brain Metastatic Progression in ER+ Breast Cancer. Role: Co-Inv