Overview
The main focus of my research has been to define the roles of nuclear hormone receptors (NHRs) in the pathogenesis of disease, with a focus on hormone-related cancers.
During earlier stages of my research career, definition of the structural and molecular determinants of NHR receptor biology and pharmacology was the main focus. Information obtained from these studies was used to guide the development of receptor modulators for therapeutic interventions and to gain insights into the pharmacology of estrogen and androgen receptor ligands. More recently, my research has shifted to define receptor-mediated signaling pathways relevant to the pathogenesis of breast and prostate cancers. One example of this is the definition of signaling pathways downstream of the orphan nuclear receptor, estrogen-related receptor alpha (ERRα) in breast cancer. Using gene expression signature defined in breast cancer cells we demonstrated that the activity of ERRα tracks with poor prognosis in all breast cancer subtypes. We confirmed a causal role for ERRα in breast cancer growth in both cellular and xenograft models of breast cancer. More recently, we further defined the role(s) of this receptor in tumor metabolism and validated its utility as a therapeutic target in triple negative breast cancer (TNBC). In addition to the cancer cell intrinsic effects of ERRα, this receptor is also expressed in T cells and in macrophages. We are currently evaluating the impact of modulating ERRα activity in these immune cells and how that influences tumor biology.
Current Appointments & Affiliations
Recent Publications
Estrogen signaling suppresses tumor-associated tissue eosinophilia to promote breast tumor growth.
Journal Article Sci Adv · September 27, 2024 Estrogens regulate eosinophilia in asthma and other inflammatory diseases. Further, peripheral eosinophilia and tumor-associated tissue eosinophilia (TATE) predicts a better response to immune checkpoint blockade (ICB) in breast cancer. However, how and if ... Full text Link to item CiteData from Targeting CaMKK2 inhibits actin cytoskeletal assembly to suppress cancer metastasis
Other · September 16, 2024 <div>Abstract<p>Triple-negative breast cancers (TNBCs) tend to become invasive and metastatic at early stages in their development. Despite some treatment successes in early stage localized TNBC, the rate of distant recurrence remains h ... Full text CiteSupplementary Figures 1-4 and Tables 1-2 from Targeting CaMKK2 inhibits actin cytoskeletal assembly to suppress cancer metastasis
Other · September 16, 2024 <p>Contains Supplementary Figures 1-4, Supplementary Tables 1-2 and legends for Supplementary Videos 1-4</p> ... Full text CiteRecent Grants
Manipulating normal estrogen physiology as a therapeutic approach in cancer
ResearchAssociate Research Professor · Awarded by National Cancer Institute · 2023 - 2028NK cell response as a clinical differentiator of endocrine therapies
ResearchAssociate Research Professor · Awarded by Department of Defense · 2024 - 2027Targeting the LYPD3 signaling pathway in metastatic breast cancer
ResearchAssociate Research Professor · Awarded by Susan G. Komen Breast Cancer Foundation · 2018 - 2026View All Grants