Profiling of 100 non-small cell lung cancers identified numerous genetic alterations impacting fibroblast growth factor receptor 3 (FGFR3) in lung squamous cell carcinoma and a novel ALK fusion partner in lung adenocarcinoma.

An FGFR3 p.R248H mutation is involved in the carcinogenesis of a subset of lung cancers.

FGFR3 tyrosine kinase fusions are associated with aggressive molecular subtype of non-small cell lung cancer.

FGFR3-TACC3 rearrangements occur in a subset of patients with lung adenocarcinoma. Such patients should be considered for clinical trials featuring FGFR inhibitors.

We present the first actionable mutation spectrum in Indian lung cancer genome. These findings implicate FGFR3 as a novel therapeutic in lung adenocarcinoma.

Studies suggest that the protein arginine N-methyltransferase 5 (PRMT5)/miR-99 family/fibroblast growth factor receptor 3 (FGFR3) axis in regulating lung cancer progression and identifies PRMT5 as a promising prognostic biomarker and therapeutic target.

FGFR3 expression indicated an adverse prognosis for lung adenocarcinoma individuals and promoted metastatic potential of lung adenocarcinoma cells

FGFR3 circular RNA promoted non-small cell lung cancer cell invasion and proliferation via competitively combining with miR-22-3p to facilitate the galectin-1, p-AKT, and p-ERK1/2 expressions.

Fgfr3 mutation caused papilloma and promoted lung tumorigenesis in cooperation with K-Ras and beta-catenin activation, respectively.

FGFR3 overexpression in lung leads to adenocarcinoma.