Megan S. Molina, PhD, CRI-Bristol Myers Squibb Postdoctoral Fellow University of Washington Area of Research: Solid Cancers One major goal of cancer therapy is to drive elimination of tumors by harnessing the immune system. The immune system protects the body by eliminating pathogens, but it also participates in healing and tissue homeostasis. The immunological milieu of solid tumors often resembles wounded tissue and therefore skews the immune response away from cell-killing and toward reparative, wound-healing functions, thus dampening anti-tumor responses and promoting tumor growth. Numerous studies have demonstrated that potent anti-tumor activity is invoked by activating innate signaling pathways associated with infection, as these reinforce cytotoxic immune responses and relieve the immunosuppression commonly observed in tumors. These findings, while significant, have not yet gained traction in the clinical setting, in part because the administration of drugs that activate innate immunity typically cause severe systemic inflammation. The goal of Dr. Molina’s work is to develop engineered signaling proteins that activate innate sensing pathways associated with infection and precisely deploy these to tumors by engineering tumor-homing T cells to express and activate them within the TME. She hypothesizes that this strategy will overcome multiple obstacles facing the cancer field by precisely targeting innate immune activation signals to the tumor, thereby improving the potency and durability of treatments such as CAR T cells or immune checkpoint inhibition while limiting off-target effects. Dr. Molina is supported by the CRI Irvington Postdoctoral Fellowship to Promote Racial Diversity. Projects and Grants Engineering innate signaling proteins to modify the tumor microenvironment University of Washington | Solid Cancers | 2023 | Andrew Oberst, PhD
