Several selective mesenchymal–epithelial transition (MET) inhibitors have recently demonstrated favorable systemic efficacy in MET exon 14 skipping mutation-positive non-small cell lung cancer. However, there are limited data on their efficacy against central nervous system (CNS) metastasis, especially leptomeningeal seeding. Recently, we encountered a case of a 65-year-old woman who was diagnosed with metastatic lung adenocarcinoma. As routine molecular testing showed no genomic alterations, including epidermal growth factor receptor mutation and anaplastic lymphoma kinase translocation, the patient received a frontline platinum-doublet followed by paclitaxel. However, the tumor did not respond to these therapies, and her condition became deleterious owing to extensive brain and leptomeningeal metastases. Plasma genotyping revealed that the tumor harbored a MET exon 14 skipping mutation, and we started capmatinib, a selective MET inhibitor. The CNS lesions markedly decreased and the performance status of the patient dramatically improved. Our report highlights the significant CNS activity of capmatinib, even in cases of leptomeningeal metastasis. In addition, this report emphasizes the importance of the active utilization of molecular profiling to detect rare but druggable genetic alterations for the better management of patients with lung cancer.

We present the Pneumocystis pneumonia case of a 64-year-old man with no remarkable history except for hypertension, who had not undergone any treatment other than surgery. On postoperative day 7, high-resolution computed tomography findings revealed multifocal ground-glass opacifications with interlobular septal thickening in both lungs; therefore, atypical pneumonia was suspected. Polymerase chain reaction (PCR) test performed after bronchoalveolar lavage was positive for Pneumocystis jirovecii (P. jirovecii). Based on the PCR results, a final diagnosis of Pneumocystis pneumonia (PCP) was made. After treatment, he improved and was discharged. This is a unique case of PCP diagnosis in a non-immunocompromised patient, with no remarkable history except for hypertension, who had not undergone any treatment other than surgery for cancer. Thus, it is necessary to consider additional risk factors for PCP and timing of preventive treatment.

Background: Non-pharmaceutical interventions (NPIs) designed to mitigate Coronavirus disease 2019 (COVID-19) transmission significantly disrupted the seasonal circulation patterns of common respiratory viruses. Objective: This study aimed to analyze the epidemiology of respiratory virus infections and the "immunity debt" hypothesis using large-scale laboratory surveillance data. Materials and Methods: This retrospective analysis utilized data from 546,631 samples tested with the Allplex™ Respiratory Panel (Seegene Inc., Seoul, South Korea) at a referral laboratory from 1 January 2020 to 31 December 2024. Each sample was screened for 18 types of respiratory viruses, excluding severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Biodiversity of viral co-detections was assessed using Simpson’s Diversity Index. In South Korea, high-intensity social distancing was strictly implemented on 22 March 2020 and officially lifted on 18 April 2022. Results: The Simpson’s Diversity Index was 0.981 in 2020 Q1 but reached its lowest levels during the most stringent quarantine period in 2021 (Q1: 0.556, Q2: 0.534). Following the easing of NPIs, the index recovered, reaching 0.907 by 2024 Q4. Conclusions: The stringency of NPIs was inversely correlated with the diversity of respiratory viral co-detections, supporting the impact of social interventions on viral ecology. Abbreviation: NPIs, non-pharmaceutical interventions; COVID-19, Coronavirus disease 2019; SARS-CoV-2, severe acute respiratory syndrome coronavirus 2 erj;68/suppl_70/PA6120/F1 F1 F1

Background: It is imperative to identify potential prognostic markers that predict recurrence of non-small cell lung cancer (NSCLC). Reactive oxygen species modulator 1 (Romo1) is a novel protein that regulates the production of intracellular reactive oxygen species. Objective: Whether tissue Romo1 expression was associated with clinical outcomes in epidermal growth factor receptor (EGFR)-mutated and surgically resected lung adenocarcinoma. Materials and Methods: A single-centered and retrospective study included 98 patients with EGFR-mutated and surgically resected lung adenocarcinoma from July 2008 to June 2021. Romo1 expression in tumor tissues was examined by immunohistochemistry and evaluated by histologic score (H-score). Univariate and multivariate analyses were performed to identify the clinicopathologic parameters associated with disease-free survival (DFS). Results: High Romo1 expression was significantly associated with a more advanced stage (p <.0001). The median DFS of the high Romo1 group was significantly shorter than that of the low Romo1 group (31.2 vs 72.1 months, p <.0001), which is also confirmed through multivariate analysis (hazard ratio 2.63, 95% confidence interval 1.13–6.09, p = 0.0243). Conclusions: Romo1 overexpression was associated with early recurrence in surgically-resected, EGFR-mutant lung adenocarcinoma. Therefore, our data highlight that Romo1 could be a potential predictive biomarker for this patient population. Abbreviation: NSCLC= non-small cell lung cancer, Romo1= reactive oxygen species modulator 1, EGFR= epidermal growth factor receptor, H score= histologic score, DFS= disease-free survival

Background/Objective: The incidence and clinical utility of pleural tissue debris, occasionally encountered in drainage systems, have not been systematically evaluated. We aimed to determine the frequency of tissue debris detection in patients undergoing drainage for pleural effusion, and its utility for the differential diagnosis of exudative effusion and pathological diagnosis of malignant pleural effusion (MPE). Methods: This retrospective proof-of-concept analysis included 325 consecutive patients who underwent percutaneous effusion drainage. The incidence, histopathological findings, and potential predictors of tissue debris were evaluated. For patients with MPE, the adequacy of tissue for immunohistochemistry and molecular testing was evaluated, and the diagnostic sensitivity of tissue debris for MPE was calculated and compared with that of cytology with cell blocks. Results: Tissue debris was detected in 151 patients (46.5%), more frequently in exudates than in transudates (51.7% vs. 23.3%, p < 0.001), and most frequently in patients with MPE (64.6%, p < 0.001). MPE was the only independent predictor of tissue debris detection (adjusted odds ratio 5.74, 95% CI 2.25–9.31). The pathological findings of the debris were classified into metastatic carcinoma/lymphoma (49.0%), acute/chronic inflammation (30.4%), fibrinoid material with inflammation (17.2%), mesothelial reaction (2.6%), and acute suppurative pleuritis/abscess (0.7%). Among the 74 cases with MPE diagnosed using tissue debris, immunohistochemistry and molecular testing were feasible in 85.1% and 69.0% cases, respectively. Diagnostic sensitivity of tissue debris for MPE was significantly higher than that of cytology (77.9% vs. 66.3%; p = 0.035) with a combined sensitivity of 84.2%. Conclusions: Systematic collection of tissue debris, a previously underrecognized clinical specimen obtained during effusion drainage, may be highly valuable for the diagnosis of MPE and adequate for immunohistochemistry and molecular testing, reducing the reliance on invasive biopsy and supporting precise oncological decisions.