Comparative study of laparoscopic versus open radical gastrectomy in advanced gastric neuroendocrine carcinoma: Analysis from a high-volume institution.

BACKGROUND: Gastric neuroendocrine carcinomas (G-NECs) are rare. This study aimed to explore the feasibility and clinical efficacy of laparoscopic surgery in patients with advanced G-NECs. METHODS: The clinicopathological data of 175 G-NECs patients who underwent radical gastrectomy in a high-volume centre were collected. One hundred fifty-one cases with advanced G-NECs (laparoscopic gastrectomy [LG] = 30, open gastrectomy [OG] = 121) were finally selected for comparison of the short-term outcomes and oncologic efficacy. RESULTS: In the postoperative recovery, when comparing the OG group, the time to ambulation (3.2 d vs. 2.6 d, respectively, p = 0.049), the time to first flatus (4.1 d vs. 3.6 d, respectively, p = 0.050), the time to first soft diet (7.9 d vs. 6.7 d, respectively, p = 0.007), and the postoperative hospital stay (13.1 d vs. 11.4 d, respectively, p = 0.047) of the LG group were shorter. There was no significant difference in the postoperative complication rates between the OG and LG groups (19.8% vs. 23.3%, p = 0.671). The 3-year overall survival (OS) rate was 57.0% in the OG group and 64.4% in the LG group (p = 0.349). The 3-year disease-free survival (DFS) rate was 51.7% in the OG group and 57.4% in the LG group (p = 0.357). There was no significant difference in the 3-year OS and DFS rates between the LG and OG groups at each stage. The recurrence rate was 35.5% in the OG group and 33.0% in the LG group (p = 0.821). CONCLUSIONS: The short-term outcomes and oncologic efficacy of laparoscopic gastrectomy and open gastrectomy for advanced G-NECs are comparable.

The Prognosis Of Peroxiredoxin Family In Breast Cancer.

PURPOSE: PRDX (Peroxiredoxin) family has involved in breast cancer tumorigenesis from the evidence obtained from cell lines, human tissues and mouse models. Nonetheless, the diversified expression patterns, coupled with the prognostic values of PRDX family, still require explanation. This study aimed at investigating the clinical importance and biological of PRDXs in breast cancer. PATIENTS AND METHODS: Specimens of paraffin sections used for immunohistochemistry were collected from the hospital and the remaining patient information was retrieved from online databases. The expression and survival data of PRDXs in patients with breast cancer were from ONCOMINE, GEPIA, Kaplan-Meier Plotter. cBioPortal, Metascape, String, Cytoscape and DAVID were used to predict functions and pathways of the changes in PRDXs and their frequently altered neighbor genes. Immunohistochemistry was used to detect the expression of PRDXs in breast cancer. RESULTS: We discovered the expression levels of PRDX1-5 were higher in breast cancer tissues than in normal tissues, whereas the expression level of PRDX6 was observed as lower in the former one in comparison with that of the latter one. There existed a correlation between the expression levels of PRDX4, 5 and the advanced tumor stage. Survival analysis revealed that the expression of PRDXs were all associated with relapse-free survival (RFS) in all of the patients with breast cancer. Eventually, we discovered significant regulation of the cellular oxidant detoxification and detoxification of ROS by the PRDX changes, together with obtaining the core modules of genes (TXN, TXN2, TXNRD1, TXNRD2, GPX1 and GPX2) linked to the PRDX family of genes in breast cancer. CONCLUSION: The PRDX family is widely involved in the development of breast cancer and affects the prognosis of patients. The functions and pathways of the changes in PRDXs and their frequently altered neighbor genes can be further verified by wet experiments.

Myocyte enhancer factor 2D provides a cross-talk between chronic inflammation and lung cancer.

BACKGROUND: Lung cancer is the leading cause of cancer-related morbidity and mortality worldwide. Patients with chronic respiratory diseases, such as chronic obstructive pulmonary disease (COPD), are exposed to a higher risk of developing lung cancer. Chronic inflammation may play an important role in the lung carcinogenesis among those patients. The present study aimed at identifying candidate biomarker predicting lung cancer risk among patients with chronic respiratory diseases. METHODS: We applied clinical bioinformatics tools to analyze different gene profile datasets with a special focus on screening the potential biomarker during chronic inflammation-lung cancer transition. Then we adopted an in vitro model based on LPS-challenged A549 cells to validate the biomarker through RNA-sequencing, quantitative real time polymerase chain reaction, and western blot analysis. RESULTS: Bioinformatics analyses of the 16 enrolled GSE datasets from Gene Expression Omnibus online database showed myocyte enhancer factor 2D (MEF2D) level significantly increased in COPD patients coexisting non-small-cell lung carcinoma (NSCLC). Inflammation challenge increased MEF2D expression in NSCLC cell line A549, associated with the severity of inflammation. Extracellular signal-regulated protein kinase inhibition could reverse the up-regulation of MEF2D in inflammation-activated A549. MEF2D played a critical role in NSCLC cell bio-behaviors, including proliferation, differentiation, and movement. CONCLUSIONS: Inflammatory conditions led to increased MEF2D expression, which might further contribute to the development of lung cancer through influencing cancer microenvironment and cell bio-behaviors. MEF2D might be a potential biomarker during chronic inflammation-lung cancer transition, predicting the risk of lung cancer among patients with chronic respiratory diseases.

Impaired self-healing capacity in airway epithelia lacking aquaporin-3.

In this study, we utilized AQP3-knockout mice as the in vivo model and AQP3-knockdown human bronchial epithelial cells (HBECs) as the in vitro model. Airway injury was experimentally induced by intra-tracheal injection of naphthalene. HE staining, transmission and scanning electron microscope were performed to evaluate self-healing capacity in vivo. Transwell and wound-healing assays were performed to evaluate epithelial cell migration in vitro. We found that both the airway epithelial cells of AQP3-knockout mice and AQP3-knockdown HBECs exhibited an obviously impaired self-healing capacity with defective epithelial cell migration through AQP3-facilitated glycerol transport. In addition, glycerol supplementation could largely correct defective injury healing and epithelial cell migration. For the first time, we found evidence for distinct defects in AQP3-deficient airway epithelial cell migration. Mechanistic analysis showed AQP3-facillitated glycerol transport plays a role in airway epithelial self-healing after injury.