Member of the NGM438 team: as initial Research Project Co-Lead, my team guided antibody screening and discovered collagen-driven myeloid biology used to identify NGM438 as an antagonist of LAIR1-mediated immune suppression. As the current Translational Lead, I leveraged our discoveries to develop a predictive and PD biomarker strategy, wrote and co-authored multiple IND reports, made direct contributions to the clinical protocol including SOA design/indication selection/biomarker rationale, worked closely with our central and specialty labs to create our LES/LTR/LSD/Laboratory Manual, and designed/oversaw clinical assay validation and implementation. I also lead LAIR1 research which include in-house discovery efforts to understand NGM438 MOA, overseeing studies at CROs, and collaborations with external investigators.

At UCSF my primary focus was to investigate the role of both myeloid cells and vascular endothelial cells in acquired resistance to antiangiogenic therapy in diverse models of cancer including pancreatic neuroendocrine tumors, breast cancer, and glioblastoma multiforme. Using in vitro and ex vivo assays and murine tumor models, my key findings were that PI3K-signaling activated a phenotypic switch in myeloid cells that controlled therapeutic response to VEGF-blockade, and that anti-VEGF therapy cooperated with anti-PD-L1 treatment to drive high endothelial venule formation and therapeutic response. In addition to this work, I collaborated with our Radiology Department to identify MRS-detectable biomarker changes associated with early pancreatic adenocarcinoma.

During my post-doc time at UTSouthwestern, I investigated the impact of antiangiogenic therapy on disease progression in pancreatic adenocarcinoma. I found that anti-VEGF treatment induced intratumoral collagen deposition and that collagen signaling protected tumor cells from hypoxia-induced cell death. I also helped identify a link between Discoidin-Domain Receptor/collagen signaling and pancreatic adenocarcinoma progression.