BackgroundConventional bronchoscopy with brushing alone for diagnosing peripheral pulmonary lesions (PPLs) is of low sensitivity. A manual mapping method was introduced and evaluated in this study, which could be routinely applied with bronchoscopic brushing to improve the sensitivity for malignant PPLs.MethodsThis mapping method involves the bronchoscopist drawing the route with a series of bronchial opening sketches and marking the leading bronchus at every bifurcation point based on thin‐section computed tomography. This map is then used to guide bronchoscope insertion for brushing. A cross‐sectional study on the evaluation of this method for the diagnosis of malignant PPLs was conducted on patients from July 2010 to June 2013.ResultsThe sensitivity for malignant PPLs of conventional brushing, conventional brushing with mapping on a portion of patients, and conventional brushing with mapping method increased from 17.0% to 25.8% to 31.5% (P < 0.001), respectively. For lesion sizes over 3 cm, the rate of these three groups increased from 25.1% to 38.6% to 50.9% (P < 0.001), respectively. The sensitivity of this mapping method for malignant PPLs was statistically associated with lesion size, lesion character, relationship between the lesion and the leading bronchus, linear distance between the targeted bronchus and the opening of the lobe bronchus, and accessibility (P < 0.001, P = 0.039, P < 0.001, P = 0.031, and P = 0.020, respectively).ConclusionsThe manual mapping method greatly increased the bronchoscopic brushing sensitivity for malignant PPLs compared to the conventional brushing method. During routine clinical work, it is economical and convenient for guiding bronchoscope insertion.

Background Ephrin receptors (Eph) and their ligands, called ephrins, function in various disease processes. However, the expression level and prognostic value of Eph/ephrins in lung adenocarcinoma (LUAD) are still unclear. Methods The Oncomine and GEPIA databases were used to explore the differential expression of Eph/ephrins in LUAD. Kaplan–Meier plotter was selected to explore the prognostic value of Eph/ephrins. The cBioPortal database was used to analyze the genetic variation of the EFNA3 gene. Immunohistochemistry was used to analyze the expression level and clinical value of ephrin-A3 protein in clinical LUAD tissue. Weighted coexpression network analysis (WGCNA) and gene set enrichment analysis (GSEA) identified the potential regulatory mechanism of EFNA3. CCK-8 assays and colony-forming experiments were used to investigate whether EFNA3 can regulate cell proliferation ability in LUAD. Analysis of lactate, ATP, and glucose uptake levels was used to explore the effect of EFNA3 on glycolysis ability. In addition, we investigated the relationship between EFNA3 and tumor infiltrating immune cells (TIICs). Finally, the potential immunotherapy response prediction value of EFNA3 was also explored. Results In this study, we found that EFNA3 expression was significantly correlated with both overall survival (OS) and progression-free survival (PFS) in LUAD patients based on a comprehensive analysis of the Eph/Ephrin family. Next, the expression of the EFNA3 protein was increased in LUAD tissues and was designated an independent prognostic risk factor. Mechanistically, EFNA3 may be involved in nuclear division, synaptic function, and ion channel activity-related pathways. In vitro experiments confirmed the role of EFNA3 in promoting LUAD cells and showed that it could regulate glycolytic capacity. Moreover, EFNA3 was negatively associated with immunity, stromal infiltration, and several TIICs. Finally, EFNA3 was found to be positively related to multiple immunotherapy biomarkers. Conclusions In conclusion, increased EFNA3 in LUAD patients predicted worse clinical prognosis, promoted LUAD cell proliferation and glycolysis ability, and was related to immunotherapy response.

Similarities in gene expression between both developing embryonic and precancerous tissues and cancer tissues may help identify much-needed biomarkers and therapeutic targets in lung squamous carcinoma. In this study, human lung samples representing ten successive time points, from embryonic development to carcinogenesis, were used to construct global gene expression profiles. Differentially expressed genes with similar expression in precancerous and cancer samples were identified. Using a network-based greedy searching algorithm to analyze the training cohort (n = 69) and three independent testing cohorts, we successfully identified a significant 22-gene module in which expression levels were correlated with overall survival in lung squamous carcinoma patients.