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- W3023622016 abstract "INTRODUCTION AND OBJECTIVE: Inhibitor targeting fibroblast growth factor receptor (FGFR) has been authorized to treat urothelial carcinoma with sensitive FGFR abberation. Here we sought to (i) clarify the proportion of potentially actionable mutation of FGF/FGFR, and (ii) evaluate the frequency of genetic alteration related to primary resistance to FGFR inhibitor. METHODS: We retrospectively analyzed the seqencing data of 363 patients with urothelial carcinoma who had admitted to hospital from Jan. 1st 2017 to Sep. 30th 2019. Of which, 244 samples were sequenced with 417-gene panel (platform: Illumina HiSeq) by 3D Medicines Inc. RESULTS: Among 244 urothelial carcinomas having received 3DMed NGS testing, 100 tumour tissues harboured deleterious FGF/FGFR alteration (FGFR1, 19%; FGFR2, 11%; FGFR3, 42%; FGFR4, 7%; FGF3/4/19 amplification, 33%, Figure 1). Specifically, 11 fusions of FGFR were detected, inlcuding one FGFR1-ZNF280B fusion and ten FGFR3-TACC3 fusions. Most missense mutations of FGFR3 led to substitute of 248-250 or 371-373 amino acids, causing gain-of-function effect. Tumour mutational burden and PD-L1 status were similar between FGF/FGFR-mutated and WT groups (TMB: median, 9.4 vs. 10.1; PD-L1 positive rate: 30.4% [24/79] vs. 33.9% [39/115]), while microsatellite instability (MSI-H) was more likely to occur in patients with FGFR mutation (6.3% vs. 0.7%). Among these 100 samples with FGF/FGFR alteration, 53 samples harboured deleterious genetic abberation associated with primary resistance to FGFR inhibitor, including the alteration in FGFR downstream signalling (9%), other receptor tyrosine kinases (19%), and mTOR signalling (34%) (Figure 1). The most prevalent resistance-related alterations involved KRAS (6%), ERBB2 (12%), PIK3CA (14%) and TSC1 (10%) (Figure 1). CONCLUSIONS: The incidence of genomic FGF/FGFR aberration in urothelial carcinoma is approximately 41.0%. Of which, the frequency of genetic alteration related to resistance to FGFR inhibitor is practically 53.0%, including KRAS (6%), ERBB2 (12%), PIK3CA (14%) and TSC1 (10%).Source of Funding: No" @default.
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- W3023622016 date "2020-04-01" @default.
- W3023622016 modified "2023-10-16" @default.
- W3023622016 title "MP55-01 GENOMIC ABERRATION OF FGF/FGFR AND GENES RELATED TO PRIMARY RESISTANCE TO FGFR INHIBITOR IN UROTHELIAL CARCINOMA" @default.
- W3023622016 doi "https://doi.org/10.1097/ju.0000000000000924.01" @default.
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