Kathryn E. Ware

TL;DR: FGF2, FGF9 and their respective high-affinity FGFRs comprise a growth factor autocrine loop that is active in a subset of gefitinib-insensitive NSCLC cell lines.

TL;DR: It is demonstrated that EGFR TKI-induced FGFR2 and FGFR3 are capable of mediating FGF2 and FGF7 stimulated ERK activation as well as FGF-stimulated transformed growth in the setting of EGfr TKIs and suggests that treatment of NSCLC patients with combinations of EGFR andFGFR specific TKis may be a strategy to enhance efficacy of single EGFR inhibitors.

TL;DR: The HNSCC cell lines can be divided into subsets defined by sensitivity to EGFR and FGFR-specific TKIs, andFGFR inhibitors may represent novel therapeutics to deploy alone or in combination with EGFR inhibitors in H NSCC.

TL;DR: Due to the high degree of homology of FGFRs with VEGFRs and PDGFRs, FGFR-active TKIs already exist and could be rapidly advanced into clinical investigations as FGFR inhibitors as a means to expand the spectrum of NSCLC patients that can be effectively targeted with TKI-directed therapies.

TL;DR: Findings show how EGFR signaling can provide a critical adaptive survival mechanism that allows cancer cells to evade oncogene-specific inhibitors, providing a rationale to cotarget EGFR to reduce the risks of developing drug resistance.