NIH R01 · 2024
Targeting the cytokine circuitry of KRAS-driven lung cancer
The goal of this research project proposal is to co-opt dysfunctional innate immune signaling in KRAS- driven lung cancers as a therapeutic vulnerability. Specifically, my laboratory has focused for many years on targeting TBK1 to inhibit the production of cytokines and chemokines such as IL-6 and CCL5 that are pro- tumorigenic and immune suppressive. For example, TBK1 inhibition sensitizes tumors to MEK inhibition, as well as PD-1 blockade. Over the past several years it has also become increasingly apparent that viral sensing pathways, such as RIG-I/MAVS or cGAS/STING play a key role in re-directing TBK1 to activate IRF3/STAT1 and initiate a cytotoxic anti-viral response. How KRAS mutant…
From the public funding record at NIH RePORTER. Describes the funded project, not the reviews below.