The Endocrine Society’s annual Rising Star Power Talks, hosted by the Trainee and Career Development Committee, features 15 early-career and in-training members presenting three-minute research blitzes with a single changing slide and two minutes for questions. At ENDO 2026, Dillon Boulton, PhD, a postdoctoral fellow in the Department of Pathology at the University of Colorado – Anschutz Medical Campus, won the Translational Science category. This format emphasizes concise communication of high-quality science, judged by both academic and industry panelists, and is intended to increase visibility and foster collaborations for emerging investigators.
Boulton’s work centers on estrogen receptor–positive breast cancer (ER+ BC), which accounts for roughly 80% of breast cancer diagnoses. Standard treatments for ER+ BC include endocrine therapies that target estrogen receptor expression or activity (for example, fulvestrant and tamoxifen) or reduce estrogen production via aromatase inhibitors. His research specifically examines how androgens and androgen receptors (AR) modulate the tumor immune microenvironment (TIME), shifting it toward an anti-inflammatory, pro-tumor phenotype.
Using matched patient samples obtained through a recently completed collaborative Phase II clinical trial, Boulton and colleagues investigated cellular and structural immune changes associated with AR activity and with AR antagonism. The translational emphasis of his project is to identify immune-modulatory mechanisms that could be targeted to improve outcomes in persistent or metastatic ER+ BC.
Although endocrine therapies are effective for many patients with ER+ BC, a significant proportion—about 20% or more depending on nodal involvement—experience relapse with metastatic disease within 10 years of diagnosis. Metastatic ER+ BC is typically not curable, motivating efforts to develop new therapeutic approaches. Immunotherapies that have benefited patients with other tumor types have not been effective in ER+ BC to date. Boulton’s research seeks to understand the interplay between hormone signaling and immune responses in the tumor microenvironment as a route to sensitize ER+ BC to immune-based therapies.
From the clinical trial–matched samples analyzed in his laboratory, Boulton reported that antagonizing AR appeared to reinvigorate the TIME. Specific observations included a decrease in the abundance of inhibitory immune cells and an increase in structures associated with anti-tumor immunity, notably tertiary lymphoid structures. These data suggest that AR activity contributes to an immunosuppressive environment in ER+ BC and that targeting AR may alter immune composition in ways favorable to anti-tumor responses.
The presentation framed these findings as preliminary but promising, highlighting the need to delineate whether immune modulation occurs through direct AR actions in immune cells or indirectly via AR-regulated tumor-derived factors. The ultimate translational aim is to determine whether AR inhibition, or targeting downstream AR-regulated transcriptional programs, can improve responsiveness of ER+ BC to immunotherapy approaches that have so far been ineffective in this subtype.
Boulton described the Endocrine Society as an important venue for disseminating his group’s work. He noted prior publication contributions in Endocrinology and valued the opportunity to present findings at ENDO both in the three-minute Rising Star format and in a longer, 10-minute talk. He emphasized that conferences like ENDO catalyze conversations, expand networks, and enable collaborations with experts across fields. As this was his first time attending ENDO, he also highlighted the educational benefit of hearing diverse presentations about hormone actions across diseases.
Looking forward, Boulton and his team will pursue mechanistic studies to clarify how AR suppresses immune responses in ER+ BC. Key questions include distinguishing direct effects of AR within immune cells from indirect effects mediated by AR-driven tumor secreted factors. The research program aims to identify actionable targets—either AR itself or downstream transcriptional targets—that can be modulated to enhance the efficacy of immunotherapies for ER+ BC. The overarching goal remains improving outcomes and quality of life for patients with persistent or metastatic ER+ breast cancer through patient-centered translational research.