A central research theme addresses how oncogenic KRAS signaling integrates with lipid metabolism to coordinate cancer cell-intrinsic programs and microenvironmental remodeling. The group has identified key roles for signaling nodes such as ACSL3, PI3Kδ and PLCγ1 in regulating fibroblast activation, extracellular matrix deposition, and immune cell infiltration, thereby shaping desmoplasia and immune evasion across tumor types. These studies employ genetically engineered mouse models, orthotopic systems, and human tumor samples, integrated with high-dimensional technologies including imaging mass cytometry, multiplex cytokine profiling as well as spatial transcriptomics and lipidomics. By combining pharmacological interventions with spatial and functional analyses of cancer cells and the TME, the research aims to define actionable vulnerabilities and inform rational combination therapies.
In parallel, the laboratory maintains a strong translational component, incorporating patient-derived material and interdisciplinary collaborations to bridge mechanistic discoveries with therapeutic development. Collectively, the group’s work provides insight into how tumor-intrinsic and microenvironmental processes converge to sustain malignancy and limit treatment efficacy in KRAS-driven cancers.
