Research ArticleCANCER IMMUNOLOGY

Hypofractionated EGFR tyrosine kinase inhibitor limits tumor relapse through triggering innate and adaptive immunity

See allHide authors and affiliations

Science Immunology  09 Aug 2019:
Vol. 4, Issue 38, eaav6473
DOI: 10.1126/sciimmunol.aav6473

You are currently viewing the editor's summary.

View Full Text

Log in to view the full text

Log in through your institution

Log in through your institution

Enhanced inhibitor

Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR TKIs) block oncogenic receptor signaling and are used as a first-line treatment for EGFR-mutated non–small cell lung cancer. Resistance to EGFR TKIs, including the standard hyperfractionated EGFR TKI (HyperTKI) treatment, is a problem that has driven the development of next-generation inhibitors. Here, Liu et al. describe the improved efficacy of hypofractionated EGFR TKI (HypoTKI) relative to HyperTKI in triggering antitumor T cell responses and preventing relapse in a TKI-sensitive syngeneic murine tumor model through a mechanism involving the type I IFN and MyD88 signaling pathways. Coadministration of HypoTKI with an anti–PD-L1 antibody further improved antitumor responses and reduced tumor relapse, thus suggesting that this combined therapy may be a potential alternative to existing treatment regimens.

View Full Text