Construction of a predictive model of 2-3 cm ground-glass nodules developing into invasive lung adenocarcinoma using high-resolution CT.

Background: The purpose of this study was to analyze the imaging risk factors for the development of 2-3 cm ground-glass nodules (GGN) for invasive lung adenocarcinoma and to establish a nomogram prediction model to provide a reference for the pathological prediction of 2-3 cm GGN and the selection of surgical procedures. Methods: We reviewed the demographic, imaging, and pathological information of 596 adult patients who underwent 2-3 cm GGN resection, between 2018 and 2022, in the Department of Thoracic Surgery, Second Affiliated Hospital of the Air Force Medical University. Based on single factor analysis, the regression method was used to analyze multiple factors, and a nomogram prediction model for 2-3 cm GGN was established. Results: (1) The risk factors for the development of 2-3 cm GGN during the invasion stage of the lung adenocarcinoma were pleural depression sign (OR = 1.687, 95%CI: 1.010-2.820), vacuole (OR = 2.334, 95%CI: 1.222-4.460), burr sign (OR = 2.617, 95%CI: 1.008-6.795), lobulated sign (OR = 3.006, 95%CI: 1.098-8.227), bronchial sign (OR = 3.134, 95%CI: 1.556-6.310), diameter of GGN (OR = 3.118, 95%CI: 1.151-8.445), and CTR (OR = 172.517, 95%CI: 48.023-619.745). (2) The 2-3 cm GGN risk prediction model was developed based on the risk factors with an AUC of 0.839; the calibration curve Y was close to the X-line, and the decision curve was drawn in the range of 0.0-1.0. Conclusion: We analyzed the risk factors for the development of 2-3 cm GGN during the invasion stage of the lung adenocarcinoma. The predictive model developed based on the above factors had some clinical significance.

Analysis of influencing factors and a predictive model of small airway dysfunction in adults.

BACKGROUND: Small airway dysfunction (SAD) is a widespread but less typical clinical manifestation of respiratory dysfunction. In lung diseases, SAD can have a higher-than-expected impact on lung function. The aim of this study was to explore risk factors for SAD and to establish a predictive model. METHODS: We included 1233 patients in the pulmonary function room of TangDu Hospital from June 2021 to December 2021. We divided the subjects into a small airway disorder group and a non-small airway disorder group, and all participants completed a questionnaire. We performed univariate and multivariate analyses to identify the risk factors for SAD. Multivariate logistic regression was performed to construct the nomogram. The performance of the nomogram was assessed and validated by the Area under roc curve (AUC), calibration curves, and Decision curve analysis (DCA). RESULTS: One. The risk factors for small airway disorder were advanced age (OR = 7.772,95% CI 2.284-26.443), female sex (OR = 1.545,95% CI 1.103-2.164), family history of respiratory disease (OR = 1.508,95% CI 1.069-2.126), history of occupational dust exposure (OR = 1.723,95% CI 1.177-2.521), history of smoking (OR = 1.732,95% CI 1.231-2.436), history of pet exposure (OR = 1.499,95% CI 1.065-2.110), exposure to O3 (OR = 1.008,95% CI 1.003-1.013), chronic bronchitis (OR = 1.947,95% CI 1.376-2.753), emphysema (OR = 2.190,95% CI 1.355-3.539) and asthma (OR = 7.287,95% CI 3.546-14.973). 2. The AUCs of the nomogram were 0.691 in the training set and 0.716 in the validation set. Both nomograms demonstrated favourable clinical consistency. 3.There was a dose‒response relationship between cigarette smoking and SAD; however, quitting smoking did not reduce the risk of SAD. CONCLUSION: Small airway disorders are associated with age, sex, family history of respiratory disease, occupational dust exposure, smoking history, history of pet exposure, exposure to O3, chronic bronchitis, emphysema, and asthma. The nomogram based on the above results can effectively used in the preliminary risk prediction.

miR-24-3p/KLF8 Signaling Axis Contributes to LUAD Metastasis by Regulating EMT.

Reprogramming of the tumor immune microenvironment is a salient feature during metastasis in LUAD. miR-24-3p and KLF8, which are key regulators of the tumor immune microenvironment, had been proved to show metastasis-promoting property in LUAD. However, whether miR-24-3p could regulate LUAD metastasis by targeting KLF8 remains unclear. This study explored the functions and mechanisms of miR-24-3p/KLF8 signaling in advanced LUAD. The expression level of miR-24-3p and KLF8 were tested in LUAD patients, and the corelation of miR-24-3p and KLF8 was evaluated. The interaction of miR-24-3p and KLF8 was demonstrated by luciferase reporter activity assay, in vitro migration and invasion studies, and in vivo metastatic studies. miR-24-3p level was downregulated in LUAD and negatively associated with KLF8 mRNA expression. miR-24-3p controls LUAD metastasis by directly targeting KLF8 and inducing Snail and E-cadherin expressions. Targeting the miR-24-3p/KLF8/EMT axis might be of great therapeutic value to advanced LUAD patients.

[Expression of Copper-Transporting P-Type Adenosine Triphosphatase (ATP7B) Correlates with Cisplatin-Resistance in Human Lung Adenocarcinoma Cell Line A549.].

BACKGROUND: Cisplatin is the basic chemotherapy agent of lung carcinoma, and cisplatin-resistance mostly leads to the failing of chemotherapy in the patients. The aim of this study is to investigate the relationship between the expression of copper-transporting P-type adenosine triphosphatase (ATP7B) and cisplatinresistance in different cisplatin-resistant A549 cells. METHODS: Three differently cisplatin-resistant A549 sublines (A549/DDP0.5, A549/DDP1.0, A549/DDP2.0) were established from their parental human lung adenocarcinoma cell line A549 which was sensitive to cisplatin, by gradually increasing concentration of cisplatin. The resistance indexes of all the sublines were checked by MTT method. The levels of ATP7B mRNA and protein were measured by RT-PCR and Western Blot respectively in all the cell lines. RESULTS: The resistance indexes of the three cisplatin-resistant sublines were 1.7, 3.2 and 5.2 respectively (P <0.001), and the levels of ATP7B mRNA were 1.6, 4.9 and 10.1 folds compared to the parental A549 cells (P <0.001). Meanwhile, expression of ATP7B protein was enhanced in the three cisplatin-resistant sulines corresponding to their cisplatin-resistance. CONCLUSIONS: Expression of ATP7B correlates with cisplatin-resistance in A549 cells, and maybe ATP7B contributes to acquisition of cisplatin-resistance.

[Comparative Proteomic Analysis of Human Lung Adenocarcinoma Cisplatin-resistant Cell Strain A549/CDDP.].

BACKGROUND: Chemotherapy plays an important role in the comprehensive therapy of lung cancer. However, the drug-resistance often causes the failure of the chemotherapy. The aim of this study is to identify differently expressed protein before and after cisplatin resistance of human lung adenocarcinoma cell A549 by proteomic analysis. METHODS: Cisplatin-resistant cell strain A549/CDDP was established by combining gradually increasing concentration of cisplatin with large dosage impact. Comparative proteomic analysis of A549 and A549/CDDP were carried out by means of two-dimensional gel electrophoresis. The differentially expressed proteins were detected and identified by MALDI-TOF mass spectrometry. RESULTS: Eighty-two differentially expressed proteins were screened by analysis the electrophoretic maps of A549 and A549/CDDP. Six differential proteins were analyzed by peptide mass fingerprinting. Glucose regulating protein 75, ribosomal protein S4, mitochondrial ATP synthase F1 complex beta subunit and immunoglobulin heavy chain variable region were identified. All four differentially expressed proteins were over-expressed in A549/CDDP, whereas low-expressed or no-expressed in A549. CONCLUSIONS: These differentially expressed proteins give some clues to elucidate the mechanism of lung cancer cell resistant of cisplatin, providing the basis of searching for potential target of chemotherapy of lung cancer.