Feng JX, et al. J Korean Med Sci. 2017 Mar;32(3):439-447. https://doi.org/10.3346/jkms.2017.32.3.439

Third-generation epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKI) show good selectivity for classical EGFR mutated and EGFR T790M mutated non-small cell lung cancer (NSCLC). However, resistance inevitably occurs to third-generation EGFR-TKI. This study describes the real-world characteristics, efficacy, and safety of treating post-progression NSCLC with 160 mg of furmonertinib (in combination with or without anti-angiogenic agents and chemotherapy) with third-generation EGFR-TKIs. EGFR-mutated NSCLC patients with intracranial progression pattern cohort (IP cohort) or extracranial progression pattern cohort (EP cohort) were retrospectively analyzed following progression to third-generation EGFR-TKIs receiving furmonertinib 160 mg daily as second-line or later treatment in combination with or without anti-angiogenic agents and chemotherapy. Thirty-nine patients were included and categorized into two groups according to the progression pattern. Then, 22 patients in the IP cohort and 17 patients in the EP cohort, most of whom were in poor physical condition, were included and 84.6% had central nervous system metastases. In the IP cohort, the median PFS was 5.5 months (95% CI 4.67-8.72), and the median OS was 9.8 months (95% CI 7.25-11.20) for single-agent furmonertinib or combination therapy. In the EP cohort, the median PFS was 3.2 months (95% CI 2.18-4.70), and the median OS was 6.7 months (95% CI 4.99-8.75). Univariate analysis showed the association between the presence of a prior T790M mutation and a history of combined radiotherapy with longer PFS with furmonertinib (p = 0.048, p = 0.004). Overall, adverse events (AEs) of any grade occurred in 84.6% of patients (33/39), with the majority having grade 2 or lower AEs. Furmonertinib 160 mg is an optional regimen for patients with advanced NSCLC who develop resistance after treatment with third-generation EGFR-TKIs, especially those developing resistance due to the progression of intracranial lesions, with good efficacy and an acceptable safety profile that warrants further exploration.

Background. Novel coronavirus disease 2019 (COVID-19) was discovered in December 2019 and has infected more than 80 million people worldwide, and more than 50 million people have achieved a clinical cure. In this study, the pulmonary function results of patients after clinical medicine for three months were reported. Objective. To investigate the effect of COVID-19 on lung function in patients. Methods. A retrospective analysis was performed on 56 COVID-19-infected patients who were cured after the clinical treatment at Taizhou Public Health Medical Center in Zhejiang Province from January 31, 2020, to March 10, 2020. At discharge and three months after discharge, lung function was measured, including inspiratory vital capacity (IVC), forced vital capacity (FVC), forced expiratory volume in first second (FEV1), forced expiratory volume in first second to inspiratory vital capacity (FEV1/IVC), maximum mid-expiratory flow rate (MEF), peak expiratory flow rate (PEF), and carbon monoxide dispersion (DLCO). Results. At discharge, there were 37 patients (66.1%) with pulmonary dysfunction, 22 patients (39.3%) with ventilation dysfunction, 31 cases (55.4%) with small airway dysfunction, and 16 cases (28.6%) with restricted ventilation dysfunction combined with small airway dysfunction. At 3 months after discharge, 24 of the 56 patients still had pulmonary dysfunction and all of them had small airway dysfunction, of which 10 patients (17.9%) were restricted ventilation dysfunction combined with small airway dysfunction. DLCO was measured three months after discharge. Twenty-nine patients (51.8%) had mild to moderate diffuse dysfunction. All pulmonary function indexes of 56 patients recovered gradually after 3 months after release, except FEV1/IVC, and the difference was statistically significant ( < 0.05). There were 41 patients of normal type (73.2%) and 15 patients of severe type (26.8%). Among the 15 severe patients, 8 patients (53.3%) had ventilation dysfunction at discharge, 9 patients (60%) had small airway dysfunction, 4 patients (26.7%) still had ventilation dysfunction 3 months after discharge, 7 patients (46.7%) had small airway dysfunction, and 10 patients (66.7%) had diffuse dysfunction. Among the 41 common type patients, 14 patients (34.1%) had ventilation dysfunction at discharge, 22 patients (53.7%) had small airway dysfunction, 6 patients (14.6%) still had ventilation dysfunction 3 months after discharge, 17 patients (41.5%) had small airway dysfunction, and 19 patients (46.3%) had diffuse dysfunction. Patients with severe COVID-19 had more pulmonary impairment and improved pulmonary function than normal patients. Conclusion. COVID-19 infection can cause lung function impairment, manifested as restricted ventilation dysfunction, small airway dysfunction, and diffuse dysfunction. The pulmonary function of most patients was improved 3 months after clinical cure and discharge, and some patients remained with mild to moderate diffuse dysfunction and small airway dysfunction.

Rearrangements of the anaplastic lymphoma kinase (ALK) gene account for 5-6% in non-small cell lung cancer (NSCLC). ALK rearranged NSCLC is sensitive to ALK tyrosine kinase inhibitors (TKIs) but prone to drug resistance. Meanwhile, ALK rearranged NSCLC has poor response to single immunotherapy. Here we mainly describe the immune escape mechanisms of ALK mutated NSCLC and the role of related biomarkers. Additionally, we collate and evaluate preclinical and clinical studies of novel immune combination regimens, and describe the prospects and perspectives for the in vivo application of novel immune technologies in patients with ALK rearranged NSCLC.

PD-L1 is one of the current biomarkers for immune checkpoint inhibitor (ICI) therapy in patients with non-small-cell lung cancer. However, the expression of PD-L1 in the real world and its related influencing factors remain unclear. We want to observe the expression of PD-L1 in the real world and study the related influencing factors through the collection and analysis of clinical data. R software (version 4.0) was used to perform data analysis and the “corplot” package for correlation analysis. A total of 296 individuals (mean [SD] age, 67 [9] years; 23%female) were assessed. According to the expression amount of PD-L1, the cohort was divided into low nonexpression group ( , 26.7%), low-expression group ( , 49.3%), and high-expression group ( , 23.5%). Age, gender, underlying diseases, smoking status, and PD-L1 expression level were not statistically significant. We found that the expression of PD-L1 was correlated with serum albumin ( ) and pathological type ( ) and had a negative correlation with EGFR mutation but did not correlate with gender, age, smoking status, combined with underlying diseases, tumor stage, whether it was initially treated or not, sampling site, specimen type, specimen storage time, R-IFN, CD4, CD8, NLR, CRP, and LDH. The present findings indicated that serum albumin, pathological type, and EGFR mutations are associated with PD-L1 expression in patients with NSCLC, which may provide a new basis for individualized immunotherapy and need further study to confirm. The results of this study help to further reveal the actual expression of PD-L1 in non-small-cell lung cancer patients with real events.

Bacterial etiology in early re-admission patients with acute exacerbation of chronic obstructive pulmonary disease