Feasibility and efficacy of transthoracic single-port assisted laparoscopic esophagogastrectomy for Siewert type II adenocarcinoma of the esophagogastric junction.

BACKGROUND: The surgical treatment of Siewert type II adenocarcinoma of the esophagogastric junction (AEG) is controversial, and no systematic technology has been established. The aim of this retrospective study is to introduce the technology of transthoracic single-port assisted laparoscopic esophagogastrectomy. METHODS: Data from patients with Siewert type II AEG who underwent transthoracic single-port assisted laparoscopic esophagogastrectomy in Guangdong Provincial Hospital of Chinese Medicine from May 2017 to December 2020 were analyzed. RESULTS: A total of 35 patients, including 30 males and 5 females, were enrolled in this study. Eight patients underwent proximal gastrectomy while the other 27 patients underwent total gastrectomy. The median operative times were 247.5 (195.0-275.0) min and 290.0 (173.0-530.0) min for proximal and total gastrectomy, respectively. The median lower mediastinal lymph node dissection (LMLD) time was 41.5 (20.0-57.0) min and the median estimated blood loss was 100.0 (20.0-200.0) mL. The median number of harvested mediastinal lymph nodes was 5 [2-13]. Lower mediastinal lymph node metastasis occurred in 9 patients (25.7%). The lower mediastinal lymph node metastasis rate was significantly higher in patients with esophageal involvement exceeding 2 cm [>2 vs. ≤2 cm: 55.6% (5/9) vs. 15.4% (4/26), P=0.03]. The median postoperative hospital stay was 10 [6-73] days. Overall morbidity was 11.8% (4 patients), including 2 cases of pleural effusion, 1 case of pancreatic fistula, and 1 case of anastomotic leakage. CONCLUSIONS: Transthoracic single-port assisted laparoscopic esophagogastrectomy is safe and feasible. It has the advantages of reducing the difficulty of LMLD and digestive tract reconstruction.

DDX56 inhibits type I interferon by disrupting assembly of IRF3-IPO5 to inhibit IRF3 nucleus import.

Transcription factor IRF3-mediated type I interferon induction plays a role in antiviral innate immunity. However, mechanisms for the control and regulation of IRF3 nuclear import remain largely unknown. We have identified DEAD box polypeptide 56 (DDX56) as a negative regulator of virus-triggered IFN-ß induction. Overexpression of DDX56 suppressed nuclear translocation of IRF3 via disrupting the IRF3-IOP5 interaction, whereas knockdown or knockout of DDX56 had the opposite effect. In addition, the interaction between DDX56 and IRF3 increased during viral infection. We further found that the D166 site of DDX56 was essential for inhibiting IRF3 import into the nucleus. Our findings suggest that DDX56 regulates antiviral innate immunity by inhibiting the nuclear translocation of IRF3, revealing a novel mechanism of the DDX56-mediated innate antiviral response.This article has an associated First Person interview with the first author of the paper.