FGF/FGFR gene aberrations such as amplification, mutation and fusion are associated with many types of human cancers including urothelial cancer. FGFR kinase inhibitors are expected to be a targeted therapy for urothelial cancer harboring FGFR3 gene alternations. ASP5878, a selective inhibitor of FGFR1, 2, 3 and 4 under clinical investigation, selectively inhibited cell proliferation of urothelial cancer cell lines harboring FGFR3 point mutation or fusion (UM‐UC‐14, RT‐112, RT4 and SW 780) among 23 urothelial cancer cell lines. Furthermore, ASP5878 inhibited cell proliferation of adriamycin‐resistant UM‐UC‐14 cell line harboring MDR1 overexpression and gemcitabine‐resistant RT‐112 cell line. The protein expression of c‐MYC, an oncoprotein, in gemcitabine‐resistant RT‐112 cell line was higher than that in RT‐112 parental cell line and ASP5878 decreased the c‐MYC expression in both RT‐112 parental and gemcitabine‐resistant RT‐112 cell lines. Once‐daily oral administration of ASP5878 exerted potent antitumor activities in UM‐UC‐14, RT‐112 and gemcitabine‐resistant RT‐112 xenograft models without affecting body weight. These findings suggest that ASP5878 has the potential to be an oral targeted therapy against urothelial cancer harboring FGFR3 fusion or FGFR3 point mutation after the acquisition of gemcitabine‐ or adriamycin‐resistance.
We report a case of epiglottic prolapse induced by lighted stylet tracheal intubation perceived by following upper gastrointestinal endoscopy. A 68-year-old male was to undergo endoscopic mucosal resection (EMR) under general anesthesia for a superficial orolarynx cancer spreading over the root of the tongue. Because the mucosal change was so minimal, intubation was performed with a lighted stylet instead of a direct laryngoscope, to prevent its metal blade spoiling the delicate endoscopic findings. After intubation, endoscopy revealed that the epiglottis folded down completely into the laryngeal vestibule. Immediate extubation with a ventilating tube exchanger failed to turn the entrapped epiglottis back to normal, and the inlet of the larynx remained obstructed. After reintubation, the epiglottis was restored to its normal position with endoscopic forceps. The postoperative course was uneventful and he was discharged on the sixth postoperative day. Retrospective evaluation of preoperative gastrointestinal endoscopy showed the epiglottis was flat and thin enough to have a tendency to become attached to the posterior pharynx wall, even though the procedure was performed in the decubitus position. Epiglottic prolapse induced by lighted stylet tracheal intubation is a quite rare complication but we should be aware of it as a potential injury which could cause upper airway obstruction if not recognized before extubation.
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