Abstract
The reliability of the fibroblast tyrosine kinase receptor 1 (FGFR1) amplification as a biomarker for FGFR inhibitors in the squamous non-small cell lung cancer (Sq-NSCLC) is not satisfactory. There is an urgent need to comprehensively characterize genetic aberrations of the FGFRs and other oncogenesis-related genes in hope to improve predictive assessment for FGFR inhibitors and treatment outcomes. Simultaneous RNA- and DNA-based detection of gene fusions, single-nucleotide variants and deletion/insertion seems the most comprehensive and informative approach to characterize genes critically involved in Sq-NSCLC tumorigenesis and progression.
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