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Fig. 6 | Molecular Cancer

Fig. 6

From: The Impact of FGFR3 Alterations on the Tumor Microenvironment and the Efficacy of Immune Checkpoint Inhibitors in Bladder Cancer

Fig. 6

Response of CPIs According to Molecular Subtypes and FGFR3 Status. A Of 389 BLCA patients, 72 were treated with CPIs including PD-1 inhibitor pembrolizumab (n = 60) and PD-L1 inhibitor avelumab (n = 12). Oncoprint sorted by the treatment response in those 72 patients is shown. B PD-L1 combined positive score (CPS), Cell count of TIM3 + cells in high power field, and FGFR3 mRNA expression were compared according to the response to CPIs. The difference was assessed by the Mann–Whitney U test. C The Objective response rate (ORR) in 72 patients treated with CPIs according to consensus subtypes (left panel) and FGFR3 alterations (right panel). D The estimated proportion of consensus subtypes in the IMvigor210 trial (PD-L1 inhibitor atezolizumab in patients with metastatic urothelial carcinoma) [17]. Pie charts show the proportion of FGFR3 mutations (not included for FGFR3 fusions) among the subtypes. E The ORR in 274 patients treated with atezolizumab according to consensus subtypes (left panel) and FGFR3 mutations (right panel). F The ORR in the IMvigor210 trial (n = 274) and the present cohort (OMPU: n = 72) treated with CPIs in Ba/Sq subtype (left panel) and LumP subtype (right panel). Fisher’s exact test was performed to assess the difference of the ORR according to FGFR3 status. Note that the data from IMvigor210 does not include the information on FGFR3 fusions. G Differentially expressed gene (DEG) analysis between MIBC/LumP/iFGFR3 (n = 64) and MIBC/LumP/aFGFR3 (n = 19) in the present cohort

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