NIH R01 · 2025
Mutant KRAS drives human cancers from several sites, including pancreatic ductal adenocarcinoma (PDAC) and low-grade serous ovarian cancer (LGSOC). Despite the prevalence of RAS mutations in different cancers, effective RAS-targeted treatment remains a challenge. KRAS monomers form homodimers and nanoclusters in the cell membrane to optimize signaling and to transform cells efficiently. Dimerization of KRAS is required for RAS-driven transformation and cancer growth. Agents that disrupt mutant RAS dimers and clusters can block oncogenic activity. Recent evidence indicates that inhibition of RAS signaling induces autophagy and enhances the response to anti-autophagic therapy. Despite four…
From the public funding record at NIH RePORTER. Describes the funded project, not the reviews below.