Research
Wound Healing
Triple Negative Breast Cancer
Our research is focused on molecular mechanisms that subvert normal resolution steps of inflammation responses that characterize impaired wound healing; a significant unmet clinical need and burden to the healthcare system in the US. To do this, my lab has made several important contributions to the field of extracellular vesicle (EV) formation that affects EV payload and activity. The hallmarks of our EV research are our focus on: a) single EV analysis, b) rigor of EV isolations, c) engineering EVs to express defined payloads and d) testing EV activity in models of tissue repair. These approaches have led to several important advances to the EV field based on the systematic evaluation of EV heterogeneity and in vivo activity with advanced single vesicle technology and cell type-specific tools.
Breast cancer remains one of the most common and deadly cancers affecting women worldwide. Triple-negative breast cancer (TNBC), a particularly aggressive subtype comprising approximately 10% of cases, is more prone to metastasis and has a five-year survival rate under 30%. Unlike other breast cancer types, TNBC lacks effective targeted therapies or immunotherapies, presenting an urgent need for new treatment strategies. Our research is focused on enhancing the body’s immune response against TNBC by targeting a receptor called CHRNA7, which regulates inflammation and immune cell function. We have recently identified specific agonists of CHRNA7 that reprograms immune cells within the tumor microenvironment to reduce the incidence of TNBC in Preclinical models.