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Purpose: To determine the effect of general anesthesia on intraocular pressure (IOP) in children with no intraocular pathology and determine which postanesthetic time point is most predictive of preinduction IOP. Design: Prospective observational study. Participants: Children with no intraocular pathology ≤ 18 years scheduled for general anesthesia as part of their routine care followed by a pediatric ophthalmologist at Nanjing Medical University. Methods: Participants underwent a standardized general anesthetic protocol using a mask induction with sevoflurane and propofol maintenance. Intraocular pressure was measured at the following 7 time points: preinduction (taken in the preoperative area), postinduction minutes 1, 3, and 5, and postairway placement minutes 1, 3, and 5 for a total time period of 10 minutes after induction. A generalized estimating equation was used to evaluate the effect of anesthesia on IOP and the effect of patient factors (age, gender, vital signs, and airway type) on preanesthetic and postanesthetic IOP. An IOP prediction model was developed using the postanesthesia IOP measurements for predicting preinduction IOP. Main Outcome Measures: Intraocular pressure and change in IOP at prespecified time points. Results: Eighty-five children were enrolled with a mean ± standard deviation (SD) age of 7.5 ± 2.9 years. Mean ± SD preinduction IOP was 20.1 ± 3.7 mmHg. Overall, IOP was lowest at 3 minutes postinduction, decreased to a mean of 13.4 ± 3.7 mmHg (P < 0.001). After this, IOP rose 5 minutes postinduction to 16.5 ± 4.2 mmHg, which did not reach preinduction IOP levels (P < 0.001). The IOP prediction model showed that combining 1 minute postinduction and 3 minutes postairway was most predictive (R2 = 0.13), whereas 1 minute postairway was least predictive of preinduction IOP (R2 = 0.01). Conclusions: After the induction of general anesthesia in children, IOP temporarily decreases with a trough at 3 minutes postinduction before increasing and remaining stable just below preinduction levels. Intraocular pressure measurements taken 1 minute after induction with 3 minutes after airway placement are most predictive of preinduction IOP, though predictive value is relatively low. Financial Disclosure(s): Proprietary or commercial disclosure may be found in the Footnotes and Disclosures at the end of this article.

MET protooncogene (MET) alterations are known driver oncogenes in NSCLC. Since the identification of MET as a potential therapeutic target, extensive clinical trials have been performed. As a result, MET-targeted therapies, including MET tyrosine kinase inhibitors, monoclonal antibodies, and MET antibody–drug conjugates now play important roles in the standard treatment of MET-altered NSCLC; they have considerably improved the outcomes of patients with tumors that harbor MET oncogenic drivers. Although clinical agents are currently available and numerous other options are in development, particular challenges in the field require attention. For example, the therapeutic efficacy of each drug remains unsatisfactory, and concomitantly, the resistance mechanisms are not fully understood. Thus, there is an urgent need for optimal drug sequencing and combinations, along with a thorough understanding of treatment resistance. In this review, we describe the current landscape of pertinent clinical trials focusing on MET-targeted strategies and discuss future developmental directions in this rapidly expanding field.