Video-Assisted Thoracoscopic Surgery for Intralobar Pulmonary Sequestration: Wedge Resection Is Feasible in Limited Peripheral Lesions.

Objectives Pulmonary sequestration is a rare developmental abnormality of the lower respiratory system. This study aimed to evaluate the effectiveness of wedge resection compared with lobectomy for the treatment of intralobar pulmonary sequestration. Methods Video-assisted thoracic surgery (VATS) for intralobar pulmonary sequestration was performed in 26 patients in our institute between December 2006 and January 2015. Data regarding patient demographics, major complaints, diagnostic procedures, operative treatment, and treatment outcome were retrospectively analyzed. Results VATS was performed successfully in all patients. Wedge resection was performed in 7 patients and lobectomy in 19 patients. Conversion to thoracotomy was not required in any case. Statistical analysis revealed that operation duration and blood loss with wedge resection were significantly less than with lobectomy (p = 0.032 and 0.014, respectively). No significant differences were found in the mean drainage time, postoperative length of hospital stay, or complications. During our long-term follow-up, no patients had chronic cough, bloody sputum, or pneumonia. Conclusion VATS for intralobar pulmonary sequestration is feasible and safe. Lobectomy is the generally accepted operative method. However, wedge resection is a feasible alternative to lobectomy in select cases.

USP7 overexpression predicts a poor prognosis in lung squamous cell carcinoma and large cell carcinoma.

In non-small cell lung cancer (NSCLC), both USP7 expression and p53 gene status were reported to be an indicator of poor prognosis in adenocarcinoma patients; however, its roles and mechanisms in lung squamous cell carcinoma and large cell carcinoma need to be clarified. The USP7 expression was examined in NSCLC tumors (excluding adenocarcinoma), their corresponding non-tumorous tissues, and NSCLC cells. Then, the prognostic role of USP7 was analyzed in 110 NSCLC samples (excluding the adenocarcinoma). Finally, the roles and mechanisms of USP7 in the proliferation, metastasis, and invasion of a NSCLC cell were assessed using a specific vshRNA. The USP7 expression was higher in NSCLC tissues compared to non-tumorous samples, accordingly, the high level of USP7 was detected in NSCLC cell lines compared with HBE cell. After the USP7 downregulation, the H460 cells exhibited decreased metastasis/invasion in vitro and in vivo. The preliminary mechanism study indicated overexpression of USP7 might regulate the p53-MDM2 pathway by inducing the MDM2 de-ubiquitination and subsequent stabilization, which resulted in the upregulation of the Bad phosphorylation. Additionally, we also found that USP7 might induce cell epithelial-mesenchymal transition to enhance the cell invasive ability. Clinically, USP7 overexpression significantly correlated with malignant phenotype. Furthermore, the 5-year overall survival in patients with USP7(low) was higher than that of USP7(high). Multivariate analysis showed USP7 overexpression was an independent prognostic marker for these cancers. USP7 overexpression may regulate the survival and invasive properties of squamous cell carcinoma and large cell carcinoma cells, and may serve as a molecular target.

The overexpression of 14-3-3ζ and Hsp27 promotes non­small cell lung cancer progression.

BACKGROUND: The 14-3-3ζ protein has been identified as a putative oncoprotein in several cancers, including non­small cell lung cancer (NSCLC). However, the mechanisms underlying its functions have not been well defined. METHODS: Proteins that interact with 14-3-3ζ were identified through coimmunoprecipitation and mass spectrometry in NSCLC cells. The interaction of 14-3-3ζ with these molecular partners and their roles in the invasiveness and metastasis of NSCLC cells were assayed through specific disruptions in the 14-3-3ζ signaling network. In addition, the clinical implications of this 14-3-3ζ complex were examined in samples from patients with NSCLC. RESULTS: Among the identified proteins that interacted with 14-3-3ζ, there were 230 proteins in 95-D cells, 181 proteins in 95-C cells, and 203 proteins in A549 cells; and 16 interacting proteins were identified that overlapped between all cell lines. Further studies revealed 14-3-3ζ complexes within the heat shock protein 27 (Hsp27) protein and demonstrated that the interference of Hsp27 or 14-3-3ζ inhibited the invasion and metastasis of NSCLC cells. The invasive and metastatic capabilities of cells with both Hsp27 and 14-3-3ζ interference could be completely restored only by Hsp27 and 14-3-3ζ complementary DNA transfection and not by either agent alone. Clinically, the postoperative 5-year overall survival (OS) in patients who had high expression of both 14-3-3ζ and Hsp27 was significantly lower than the 5-year OS in patients who had low expression of both 14-3-3ζ and Hsp27 (26.5% vs 59.7%, respectively). Multivariate analysis revealed that the combined expression of 14-3-3ζ and Hsp27 was an independent prognostic indicator of OS(P = .036). CONCLUSIONS: The current data suggest that the combined expression of 14-3-3ζ and Hsp27 may be a biomarker for predicting survival in patients with NSCLC, and this combination may have potential as a therapeutic target for NSCLC.

Genome-wide screening and co-expression network analysis identify recurrence-specific biomarkers of esophageal squamous cell carcinoma.

Tumor recurrence and metastasis after surgery are the leading causes of death in patients with esophageal squamous cell carcinoma (ESCC). Next-generation sequencing techniques have improved our understanding of the genetic alterations underlying tumor initiation and progression. To explore recurrence-specific transcriptional profiles, functional properties, and gene co-expression networks in ESCC, samples from recurrence (n = 4) and nonrecurrence (n = 4) groups were analyzed by RNA sequencing. Patients included in the nonrecurrence group had five or more years of survival without any evidence of recurrence or metastasis, while those included in the recurrence group exhibited early recurrence and metastasis and died within 2 years. We identified 533 significantly differentially expressed protein-coding and noncoding genes. Functional enrichment analysis indicated that ESCC recurrence was related to dysregulated cell-cell adherence, microenvironment homeostasis, information processing, and the immune response. Co-expression networks demonstrated differences in the patterns of gene expression and co-expression between the recurrence and nonrecurrence groups. This study provided important insights into ESCC progression and the differentially expressed genes that may represent potential targets for ESCC diagnosis and therapy.

Submucosal Tunneling Endoscopic Resection vs Thoracoscopic Enucleation for Large Submucosal Tumors in the Esophagus and the Esophagogastric Junction.

BACKGROUND: Submucosal tunneling endoscopic resection (STER) is regarded as a promising method for resection of submucosal tumors (SMTs); however, little is known about a comprehensive comparison of STER and thoracoscopic enucleation (TE). The aim of this study was to compare the clinical outcomes of STER and TE for large symptomatic SMTs in the esophagus and esophagogastric junction, as well as to analyze the factors that affect the feasibility and safety of STER. STUDY DESIGN: We enrolled 166 patients with large symptomatic SMTs in the esophagus and esophagogastric junction from September 2011 to March 2016 in this retrospective study. The clinicopathologic features and treatment results were collected and analyzed. RESULTS: En bloc resection was achieved in 84.6% of the patients in the STER group and 86.7% of the patients in the TE group (p = 0.708). Notably, the procedure time and hospital stay in the STER group were considerably shorter than those in the TE group. Tumor transverse diameter is a significant risk factor for piecemeal resection, adverse events, and technical difficulties. No recurrence or metastasis was found during a mean follow-up period of more than 2 years. CONCLUSIONS: Submucosal tunneling endoscopic resection is effective and safe for large SMTs in the esophagus and esophagogastric junction. This procedure has the advantage of being more minimally invasive with a shorter procedure time and hospital stay compared with TE. Submucosal tunneling endoscopic resection for tumors with a transverse diameter ≥3.5 cm and an irregular shape is associated with relatively high risk for piecemeal resection, adverse events, and technical difficulties.

Uniportal video-assisted thoracic lobectomy in a semiprone position for the treatment of a large intralobar pulmonary sequestration.

Intralobar pulmonary sequestration (IPS) is a rare developmental abnormality of the lower respiratory system. Lobectomy by video-assisted thoracic surgery using a three-port or four-port technique is the generally accepted operative approach. However, lobectomy can also be accomplished with a single incision even if the IPS is large. This report describes the first case of a patient with a large IPS undergoing uniportal video-assisted thoracic lobectomy in a semiprone position.

Capn4 promotes non-small cell lung cancer progression via upregulation of matrix metalloproteinase 2.

The expression of calpain small subunit 1 (Capn4) is correlated with the invasion of several types of tumors. However, the roles of Capn4 in non-small cell lung cancer (NSCLC) remain unclear. In this study, we found that the expression of Capn4 in NSCLC tissues was much higher than that in nontumorous samples. High levels of Capn4 expression were associated with lymph node metastasis and large tumor size in NSCLC patients. The 5-year overall survival rate in the Capn4(high) group was significantly lower than that in the Capn4(low) group. In multivariate analysis, Capn4 was identified as an independent prognostic factor for overall survival. Moreover, in an in vitro analysis, downregulation of Capn4 expression by siRNA suppressed the invasive potential of lung cancer cells. Finally, we demonstrated that Capn4 enhanced the invasion ability of lung cancer cells by upregulating the expression of matrix metalloproteinase 2. Our findings indicated that Capn4 may represent a potential therapeutic target and a novel prognostic marker of NSCLC.

Overexpression of CD88 predicts poor prognosis in non-small-cell lung cancer.

CD88 (C5aR), a G-protein-coupled receptor, is well known as it functions in various inflammatory diseases, however, its role in tumorigenesis remains unclear. In this study we investigated the prognostic value of CD88 in patients with non-small-cell lung cancer (NSCLC) after surgical resection. Five NSCLC cell lines and one normal bronchial epithelial cell line were used to analyze the CD88 expression at the mRNA level. Then, the expression of CD88 and E-cadherin were further examined by immunohistochemistry (IHC) in tissue microarray (TMA) consisting of 208 cases of NSCLSs. Data revealed that CD88 expression was significantly higher in NSCLC cells than that in normal bronchial epithelial cells, and compared with the adjacent non-tumorous lung tissues, the CD88 protein overexpressed in NSCLC tissues. Furthermore, high levels of CD88 were found to be correlated with lymph node metastasis in NSCLC patients (p = 0.012). The 5-year overall survival of patients with CD88(high) was significantly lower than those in the CD88(low) group (p = 0.001), and multivariate analysis revealed that CD88 expression was an independent prognostic factor in patients' overall survival (HR = 1.614, 95% CI 1.082-2.407, p = 0.019). Finally, we confirmed the CD88 expression negatively correlated with E-cadherin expression (p < 0.001). Interference of CD88 expression impaired the migration of lung cancer cells and up-regulated the E-cadherin protein expression. Thus, our results indicate that CD88 is overexpressed in NSCLC. High levels of CD88 are associated with poor prognosis of NSCLC after resection and promote tumor metastasis via down-regulation of E-cadherin. CD88 can be a potential prognostic marker to screen patients for unfavorable prognosis.

[Video-assisted thoracoscopic surgery in the treatment of esophageal leiomyoma: a report of 39 cases].

OBJECTIVE: To investigate the application and efficacy of video-assisted thoracoscopic surgery in the treatment of esophageal leiomyoma. METHODS: Clinical data of 39 patients with esophageal leiomyoma from December 2002 to November 2008 treated by video-assisted thoracoscopic surgery were reviewed retrospectively. RESULTS: Video-assisted thoracoscopic leiomyoma enucleations were performed in 38 patients, and one patient was converted to thoracotomy to repair the esophageal mucosa because of mucosa rupture during the operation. Thirty-six patients were treated through the right chest and the other 3 cases through the left. The operation time ranged from 1 to 5 (1.2+/-0.6) h. The blood loss ranged from 30 to 100 (50+/-8.3) ml. The time of chest tube placement ranged from 1 to 4 (1.5+/-0.7) d. The drainage amount was 100 to 500 (200+/-101) ml. The hospital stay ranged from 3 to 10 (3.6+/-1.2) d. The maximal diameter of the tumor ranged from 0.8 to 6.0 (3.0+/-0.7) cm. There were no surgery-related complications or deaths except the case with esophageal mucosa rupture. There were no uncomfortable complains and tumor recurrence within the follow-up period of 1 to 72 months after operation. CONCLUSION: Video-assisted thoracoscopic leiomyoma enucleation is a safe and effective approach for esophageal leiomyoma.