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FGFR1 and FGFR2 are amplified in many tumour types, yet what determines response to FGFR inhibition in amplified cancers is unknown. In a translational clinical trial we show that gastric cancers with high-level clonal FGFR2 amplification have a high response rate to the selective FGFR inhibitor AZD4547, whilst cancers with sub-clonal or low-level amplification did not respond. Using cell lines and patient derived xenografts models, we show high-level FGFR2 amplification initiates a distinctdoi:10.1158/2159-8290.cd-15-1246 pmid:27179038 pmcid:PMC5338732 fatcat:razilydc4jclnfu5p4t62lnnbm