I connect oncology biology, biomarker strategy, assay validation, and preclinical research to support rigorous diagnostic and therapeutic development.

Supported early-stage small-molecule development in women's health, spanning assay strategy, pharmacology, lead optimization, and nonclinical planning. Developed translational assays and preclinical study strategies supporting compound characterization and candidate selection, contributed to nonclinical and IND-enabling planning including study design, budget estimates, and external-study coordination, and helped establish laboratory workflows, vendor relationships, and scientific documentation for an early-stage biotechnology company.

Led preclinical drug-discovery efforts in pancreatic ductal adenocarcinoma (PDAC) to improve the efficacy of epigenetic therapies and immune checkpoint inhibitors. Built multi-cell co-culture systems modeling the tumor–immune microenvironment, executed orthotopic in vivo studies with survival endpoints, and integrated flow cytometry, cytokine profiling, and RNA-seq. Showed that low-dose dual epigenetic therapy combined with anti–PD-1 reverses an HMA-induced suppressive myeloid phenotype and prolongs survival in an orthotopic PDAC model.

Led NSCLC studies that uncovered a previously unrecognized role for the CTLH E3 ubiquitin ligase complex (the RANBP9/RANBP10 "rheostat") in tumor progression and therapy resistance. Generated multiple GEMMs and 20+ stable isogenic cell lines powering mechanistic studies and high-throughput screening; findings established RANBP9/RANBP10 as candidate therapeutic targets and linked RANBP9 to platinum sensitivity and a PARP-inhibitor "BRCAness-like" vulnerability.

Identified AGC-family kinases, notably SGK1, as essential, AKT-independent drivers of PI3K-driven thyroid cancer survival. Established primary thyrocyte cultures, generated 20+ engineered cell lines, and supported 100+ in vivo and in vitro studies, including industry collaborations to screen and validate small-molecule kinase inhibitors.