Yuanzhen Hao, Yining Wang, Miao Qi, Xin He, Ying Zhu, and Junbo Hong. Gut and Liver 1999;0:. https://doi.org/10.5009/gnl19097

Background: Endoscopic resection has been increasingly adopted for neoplasms in the major duodenal papilla. Previous studies have reached varying conclusions on whether prophylactic pancreatic stent (PS) placement is an effective measure against post-procedure complications. We aimed to investigate whether PS could reduce the incidence of post-procedure complications. Methods: The PubMed, Cochrane Library, and EMBASE databases were systematically searched from the inception dates to 25 December 2018 to identify all randomized controlled trials (RCTs) and retrospective cohort studies (RCSs) comparing prophylactic PS and no PS against post-procedure complications. The main outcomes measurements were post-procedure pancreatitis, bleeding, perforation and late papillary stenosis. Results: 23 RCSs (1001 subjects) and 2 RCTs met the inclusion criteria. Meta-analysis of the RCSs showed that prophylactic PS decreased the odds of post-procedure pancreatitis (OR, 0.71; 95% CI, 0.36–1.40; p = 0.325) as well as late papillary stenosis (OR, 0.35; 95% CI, 0.07–1.75; p = 0.200; I² =0%) and increased the odds of bleeding (OR, 1.32; 95% CI, 0.50–3.46; p = 0.572; I² = 0%) and perforation (OR, 2.25; 95% CI, 0.33–15.50; p = 0.412; I² = 0%) but not significantly. Sensitivity analysis illustrated prophylactic PS significantly decreased the risk of post-procedure pancreatitis (OR, 0.44; 95% CI, 0.24–0.80; p = 0.007). Conclusions: PS placement was prophylactic against post-procedure complications although not significantly. Sensitivity analysis suggests the significant effect of prophylactic PS against post-procedure pancreatitis. More RCTs are required to validate the statistical significance of our results and potentially relevant characteristics improving the prophylactic efficacy of stents.

N1-methyladenosine (m1A) and long non-coding RNAs (lncRNAs) play significant roles in tumor progression in hepatocellular carcinoma (HCC). However, their association with HCC is still unclear. In this study, lncRNAs related to m1A were extracted from the mRNA expression matrix in The Cancer Genome Atlas (TCGA) database. Five m1A-related lncRNAs (AL031985.3, NRAV, WAC-AS1, AC026412.3, and AC099850.4) were identified based on lasso Cox regression and they generated a prognostic signature of HCC. The prognostic signature was identified as an independent prognosis factor in HCC patients. Moreover, the prognostic signature achieved better performance than TP53 mutation status or tumor mutational burden (TMB) scores in the stratification of patient survival. The immune landscape indicated that most immune checkpoint genes and immune cells were distributed differently between both risk groups. A higher IC₅₀ of chemotherapeutics (sorafenib, nilotinib, sunitinib, and gefitinib) was observed in the high-risk group, and a lower IC₅₀ of gemcitabine in the low-risk group, suggesting the potential of the prognostic signature in chemosensitivity. In addition, fifty-five potential small molecular drugs were found based on drug sensitivity and NRAV expression. Together, five m1A-related lncRNAs generated a prognostic signature that could be a promising prognostic prediction approach and therapeutic response assessment tool for HCC patients.

Background. It was gradually accepted that endoscopic fragment biopsy (EFB) diagnosis cannot accurately guarantee the absence of higher‐grade neoplasms within the lesion of the digestive tract. There are no well‐established predictors for histopathologically upgrade discrepancies between EFB diagnosing colorectal low‐grade intraepithelial neoplasia (LGIN) and endoscopic resection (ER) specimens. Methods. A total of 918 colorectal LGINs was histopathologically diagnosed by EFB, including 162 cases with upgrade discrepancy and 756 concordant cases. We compared clinicopathological data of EFB and ER specimens between these two groups. Multivariate analysis was performed to identify predictors for this upgrade histopathology. Results. The predominant upgrade discrepancy of LGINs diagnosed by EFB was upgrades to high‐grade dysplasia (114/918, 12.4%), followed by upgrades to intramucosal carcinoma (33/918, 3.6%), submucosal adenocarcinoma (10/918, 1.1%), and advanced adenocarcinoma (5/918, 0.5%). NSAID history (OR 4.83; 95% CI, 2.27‐10.27; p < 0.001), insufficient EFB number (OR 2.99; 95% CI, 1.91‐4.68; p < 0.001), maximum diameter ≥ 1.0 cm (OR 6.18; 95% CI, 1.32‐28.99; p = 0.021), lobulated shape (OR 2.68; 95% CI, 1.65‐4.36; p < 0.001), erythema (OR 2.42; 95% CI, 1.50‐3.91; p < 0.001), erosion (OR 7.12; 95% CI, 3.91‐12.94; p < 0.001), surface unevenness (OR 2.31; 95% CI, 1.33‐4.01; p = 0.003), and distal location of the target adenoma (OR 3.29; 95% CI, 1.68‐6.41; p < 0.001) were associated with the histologically upgrade discrepancies. Conclusion. NSAID history, insufficient EFB number, adenoma size and location, and abnormal macroscopic patterns are potential predictors for upgrade histopathology of LGINs diagnosed by EFBs. The standardization of EFB number and advanced imaging techniques could minimize the risk of neglecting the potential of this upgrade histopathology.