Cancer cells undergo profound oncogene-driven reprogramming to meet the metabolic and biosynthetic demands of uncontrolled growth, survival, and proliferation. Our lab investigates how this transformation creates unique vulnerabilities in cancer cells—vulnerabilities that can be targeted to develop innovative therapeutic strategies.
We focus on KRAS-driven lung and pancreatic adenocarcinomas, two aggressive cancer types characterized by poor prognosis and limited treatment options. A major aim of our research is to understand how KRAS alters intracellular signaling pathways and lipid metabolism to support tumor progression, adaptation, and resistance to therapy.
To address these questions, we employ a multidisciplinary approach that integrates molecular biology, cell biology, and biochemistry. Our experimental systems include established and primary cancer cell lines, genetically engineered mouse models of lung and pancreatic cancer, as well as human tumor specimens, including patient-derived tissues, tissue microarrays (TMAs), and other clinically annotated samples.
We leverage spatial lipidomics and transcriptomics to map metabolic and gene expression changes within the tumor microenvironment at high spatial resolution, providing deeper insights into tissue architecture, tumor heterogeneity, and cellular interactions. A key area of interest is how metabolic rewiring contributes to drug resistance, with the goal of identifying new combination strategies that overcome therapeutic failure.
Through this comprehensive and translational research pipeline, we aim to bridge fundamental mechanistic insights with clinical relevance to advance the next generation of targeted cancer therapies.
