Research trends on endoscopic mucosal resection: A bibliometric analysis from 1991 to 2021.

Background: In recent years, the rapid development of digestive endoscopy technology has brought revolutionary changes to endoscopic therapy. A growing number of articles have been published annually. We aimed to explore global scientific outputs and hotspots of endoscopic mucosal resection (EMR) published by different countries, organizations, and authors. Methods: We extracted relevant publications from the Web of Science Core Collection (WOSCC) on June 23, 2022. We examined the retrieved data by bibliometric analysis (e.g., cocited and cluster analysis, keyword co-occurrence) using the software CiteSpace and VOSviewer to analyze and predict the trends and hot spots in this field. Results: A total of 2,695 papers were finally identified. The results showed that the number of articles fluctuated with the year and reached its peak in 2021. NATIONAL CANCER CENTER JAPAN was the most influential institution. MICHAEL J BOURKE and YUTAKA SAITO are two of the most prolific scholars. ENDOSCOPY and GASTROINTESTINAL ENDOSCOPY were the most productive journals. "Early gastric cancer" and "Barrett's esophagus" were the focus of EMR research. "Adverse events", "cold snare polypectomy" and "outcomes" have become increasingly popular in recent years and could become hot spots in the future. Conclusion: In this study, we summarized the characteristics of the publications; identified the most influential countries, institutions, and journals; and identified the leading topics in the EMR field.

U2AF1 mutation connects DNA damage to the alternative splicing of RAD51 in lung adenocarcinomas.

The recurrent mutation (S34F) in splicing factor U2AF1 is frequently observed in lung adenocarcinoma, but its function remains largely unknown. To determine the mechanistic basis and consequences of U2AF1 mutations, we established non-small cell lung carcinoma A549 cell lines with exogenous expression of wildtype (U2AF1-WT) or mutant (U2AF1-S34F). Splicing analysis revealed that U2AF1-S34F mainly caused aberrant exon usage and affected splicing of numerous DNA damage repair genes. Compared to A549 cells expressing U2AF1-WT, cells expressing U2AF1-S34F showed enhanced DNA damage and cell death in response to ATR inhibitors (ATRi). Mechanistically, U2AF1-S34F induced mis-splicing and downregulation of a key homologous recombination protein RAD51. Overexpression of RAD51 could largely rescue the defective DNA damage response in cells expressing U2AF1-S34F. Moreover, A549 cells expressing U2AF1-S34F, but not U2AF1-WT, were highly sensitive to treatment even with low dose of RAD51 inhibitor on ATRi-induced DNA damage. Our results suggest that U2AF1-S34F causes mis-splicing of DNA damage repair factors in lung cancer and sensitizes cells to RAD51 inhibition.