Background: Thoracic wall tumors can leave large defects in the thoracic wall after tumor resection. Currently, the shape of the materials commonly used for thoracic wall repair, including dacron mesh and titanium alloy mesh, cannot readily conform to the shapes of defect sites. In this study, we aimed to retrospectively review and evaluate the outcomes of applying three-dimensional (3D) printing technology in assisting in thoracic wall tumor resection and thoracic wall construction. Methods: Six patients with thoracic wall tumors underwent thin-slice CT scanning. We 3D reconstructed pleural tumors and adjacent structures with Amira software and 3D printed them. Preoperative simulation, surgical rehearsal, and surgical planning were performed, and 3D conformal titanium plates were created based on 3D reconstruction models and sutured to the defect sites of the thoracic wall. We also retrospectively reviewed 10 patients who underwent this surgery with conventional methods. All of the demographic data, clinical data, and laboratory findings (non-normally distributed variables) were compared between these two groups. Results: 3D reconstructions of the tumors and their adjacent structures were successfully performed, and 3D printing physical models and conformal titanium plates were also successfully obtained. The plate afforded accurate matching, less bleeding, fewer postoperative complications, and less pain. Conclusions: This 3D printing technology can aid in preoperative rehearsal, surgical planning, and the manufacturing of 3D implants. The 3D titanium plate has such advantages over traditional implants as having good fit and hardness, improving the surgical accuracy and curative effect, and reducing complications, such as bleeding and pain.

Radiotherapy (RT) is one of the important treatment modalities for non-small cell lung cancer (NSCLC). However, the maximum radiation dose that NSCLC patient can receive varies little. Therefore, the exploitation of novel RT sensitization approaches is a critical need for the clinical treatment. RT resistance in NSCLC is linked to tumor microenvironment (TME) hypoxia, cell cycle arrest and associated genetic alterations. Here, we designed a novel method for targeted delivery of quercetin (QT) and CeO₂ to enhance RT sensitivity. We loaded QT into CeO₂@ZIF-8-HA nanoparticles to prevent its degradation in the circulatory system and successfully delivered QT and CeO₂ targeted to NSCLC tumors. Under the protection and targeted delivery of Zeolitic Imidazolate Framework-8 (ZIF-8), the nanocomplexes exhibited excellent catalytic mimetic activity in decomposing H₂O₂ into O₂, thus significantly reversing the hypoxia of TME, while the radiosensitizer QT caused DNA damage directly after RT. In a subcutaneous tumor model, CeO₂@ZIF-8-HA overcame radiation resistance and enhanced therapeutic efficacy. This multiple sensitization strategy combining delivery of QT and CeO₂@ZIF-8-HA nanozymes opens a promising approach for RT of NSCLC.

Background: Pulmonary sequestration (PS) is a rare congenital pulmonary malformation. In this study, we aimed to retrospect and evaluate the diagnosis, treatment, and outcomes of PS in 28 patients at our institute. Methods: The files of 28 patients with PS who were treated with surgery (21 cases) or endovascular intervention (7 cases) between May 2005 and June 2016 from a single institute were retrospectively reviewed. The following data of all patients were analyzed: age, sex, clinical symptoms, diagnostic methods, operative techniques, and treatment outcomes. Results: Twenty-eight patients, 15 male and 13 female, with a median age of 42.5 underwent operative intervention for PS. Twenty-one patients showed preoperative symptoms including cough, expectoration, hemoptysis, chest and/or back pain, and fever. General chest computed tomography (CT) scanning; percutaneous needle biopsy, bronchoscopy, enhanced CT scanning, and CT angiography (CTA) were used as diagnostic methods. Twenty-one patients were diagnosed preoperatively by enhanced CT scanning and CTA; seven patients were confirmed by surgery. Twenty-one patients underwent surgery (15 cases via thoracotomy and 6 cases via video-assisted thoracic surgery), seven patients underwent interventional therapy (three cases via endovascular embolization and four cases via thoracic aortic endovascular stent-graft exclusion). Three patients had a complication in surgery group (intraoperative hemorrhage in two patients and postoperative hydropneumothorax in one patient) and two patients had post-embolization syndrome in interventional group (fever and pain at embolism site). During the follow-up period ranging from 6 to 84 months, no recurrences or further complications were observed in two groups. Conclusions: Enhanced CT or CTA may be a potential approach for the diagnosis of PS. Surgical resection for PS is the major treatment approach. Endovascular embolization of PS could be considered when pulmonary lesion is small-sized. Endovascular exclusion could be used to treat combined arterial aneurysm and dissection of PS.

Purpose: Centromere protein U (CENPU) abnormally exhibits high expression in various types of human tumor tissues and participates in tumor progression; however, its expression pattern and biological function in lung cancer have not yet been elucidated. In the present study, we explored the clinical significance and biological function of CENPU in lung cancer. Materials and methods: The Cancer Genome Atlas (TCGA) data analyses, quantitative real-time PCR (RT-PCR), and Western blotting were performed to quantify CENPU and FOXM1 expression in non-small-cell lung cancer (NSCLC) samples. Survival data were obtained from Kaplan–Meier plotter or PROGgene V2 prognostic database. The function of CENPU in lung cancer cell proliferation was determined using 5-ethynyl-2′-deoxyuridine (EdU), Cell Counting Kit-8 (CCK-8), and cell cycle assays, and the underlying mechanism was determined through bioinformatic analyses and validated by in vitro siRNA or plasmid transfection experiments. Results: CENPU was abnormally overexpressed in NSCLC samples compared with matched paired normal tissues. Higher expression of CENPU predicted worse overall survival (OS) and relapse-free survival (RFS) in NSCLC patients. Knockdown of CENPU expression by siRNA significantly inhibited proliferation and delayed cell cycle progression of lung cancer cells. To figure out the mechanism, bioinformatic analyses were performed and the results showed that the transcription factor, FOXM1, positively correlated with CENPU. Further in vitro experiments indicated that FOXM1 was the possible downstream transcription factor of CENPU as the knockdown of CENPU led to lower expression of FOXM1 and the overexpression of FOXM1 significantly reversed the inhibition of proliferation caused by CENPU knockdown. Furthermore, FOXM1 was highly expressed in NSCLC. The knockdown of FOXM1 also attenuated proliferation and induced G1 arrest in lung cancer cells. Conclusion: CENPU was highly expressed in NSCLC tissues, wherein it promoted lung cancer cell proliferation via the transcription factor, FOXM1, which could be a potential target for therapeutic strategies.

A postoperative comparison of high-flow nasal cannula therapy and conventional oxygen therapy for esophageal cancer patients Mei Xia, Weina Li, Jie Yao, Ying Jin, Gaoli Du, Qianfeng Xu, Xing Yi, Xiaoxia Nv, Yi Wu, Ping He, Wei Wu

Background/Aim: Fas/FasL system is a major regulator of apoptosis. The mechanisms by which Fas mediates cisplatin resistance remain unclear. The aim of this study is to explore the effect of Fas over-expression on cisplatin resistance of small cell lung cancer cells and its possible mechanisms.Materials and methods: Fas was over-expressed in H446/CDDP cells by infection with the adenoviruses containing Fas. Sensitivity of Fas-overexpressed H446/CDDP cells to cisplatin was evaluated using MTT assay. Expressions of Fas, GST-π and ERCC1 were detected by RT-PCR and Western blot analysis. Apoptosis rate was examined by FACS.Results: Over-expression of Fas in H446/CDDP cells significantly decreased the expressions of GST-π and ERCC1 at mRNA and protein levels, and increased the cell apoptosis. Furthermore, up-regulation of Fas significantly decreased the tolerance of H446/CDDP cells to cisplatin.Conclusion: Over-expression of Fas reverses drug resistance of H446/CDDP cells, possibly due to the increased cell sensitivity to apoptosis and the decreased expressions of GST-π and ERCC1.