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Objective: To investigate the clinical potential and safety of Moluodan to reverse gastric precancerous lesions., Methods: Patients aged 18-70 years diagnosed with moderate-to-severe atrophy and/or moderate-to-severe intestinal metaplasia, with or without low-grade dysplasia, and negative for Helicobacter pylori were recruited in this randomized, double-blind, parallel-controlled trial. The primary outcome was the improvement of global histological diagnosis at 1-year follow-up endoscopy using the operative link for gastritis assessment, the operative link for gastric intestinal metaplasia assessment, and the disappearance rate of dysplasia., Results: Between November 3, 2017 and January 27, 2021, 166 subjects were randomly assigned to the Moluodan group, 168 to the folic acid group, 84 to the combination group, and 84 to the high-dose Moluodan group. The improvement in global histological diagnosis was achieved in 60 (39.5%) subjects receiving Moluodan, 59 (37.8%) receiving folic acid, 26 (32.1%) receiving the combined drugs, and 36 (47.4%) receiving high-dose Moluodan. Moluodan was non-inferior to folic acid (95% confidence interval: -9.2 to 12.5; P = 0.02). High-dose Moluodan had a trend for better protective efficacy, though there was no statistical significance. The disappearance rate of dysplasia was 82.8% in the Moluodan group, which was superior to folic acid (53.9%; P = 0.006). No drug-related serious adverse events were observed., Conclusions: One pack of Moluodan three times daily for 1 year was safe and effective in reversing gastric precancerous lesions, especially dysplasia. Doubling its dose showed a better efficacy trend., (© 2024 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and John Wiley & Sons Australia, Ltd.)

Objective: Serrated polyps (SP) are regarded as precursor lesions of colorectal cancer (CRC). We conducted this single-center study aiming to investigate the relationship between SP and synchronous and metachronous advanced neoplasia in the Chinese population., Methods: The data for this retrospective study were collected from the Endoscopy Center and Department of Gastroenterology of Renji Hospital, School of Medicine, Shanghai Jiao Tong University between May 2012 and May 2019. Altogether 2205 patients were pathologically confirmed with colorectal SP., Results: The detection rate of SP among all polyps has gradually increased since 2014 and reached 8.74% by 2019. Among all the SP cases, 1540 (69.84%) were confirmed as having hyperplasic polyps (HP), 486 (22.04%) were having sessile serrated lesions (SSL), and 171 (7.76%) had traditional serrated adenomas (TSA). Compared with HP (2.14%), SSL and TSA were larger and more likely to be accompanied by synchronous and metachronous advanced neoplasia (6.79% and 6.08%). We next found that large SP (diameter ≥10 mm) (odds ratio [OR] 2.52, 95% confidence interval [CI] 1.40-4.55, P = 0.002) and SSL with high-grade intraepithelial neoplasia (OR 13.85, 95% CI 3.28-58.56, P < 0.001) were associated with an increased risk of synchronous advanced neoplasia. However, we failed to find a relationship between SP and metachronous advanced neoplasia because few patients had developed metachronous advanced neoplasia., Conclusion: Large SP and SSL with high-grade intraepithelial neoplasia are associated with synchronous advanced neoplasia and require timely surveillance., (© 2020 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and John Wiley & Sons Australia, Ltd.)

Objective: To investigate the molecular mechanism of colorectal cancer (CRC) cell apoptosis induced by the Jumonji domain containing 2B (JMJD2B) silencing., Methods: Both HCT116 and LoVo CRC cell lines were used for analyses. Cell apoptosis after JMJD2B silencing was determined by flow cytometry. JC-1 fluorescence probe was applied to measure the mitochondrial outer membrane permeabilization by flow cytometry and fluorescence microscopy. Immunofluorescence was used to detect cytochrome C translocation from mitochondria to cytosol after JMJD2B silencing. The efficacy of JMJD2B silencing on the protein levels of Bcl-2 family, caspase proteins, CCAAT/enhancer binding protein homologous protein (CHOP) and glucose-regulated protein 78 (GRP78) were detected by Western blot., Results: JMJD2B silencing induced CRC cell apoptosis via a decrease of the anti-apoptotic gene Bcl-2 family expression, leading to the translocation of Bak and Bax proteins and the promotion of mitochondrial membrane disruption, resulting in the release of cytochrome C from mitochondria and subsequent caspase-9 and caspase-3 cleavage. It also increased the amount of cleaved caspase-8 involved in the death receptor-related apoptotic pathway. Bcl-2 homology 3 interacting-domain death agonist (Bid), a specific caspase-8 substrate involved in the Fas signaling pathway, subsequently induced cleavage via caspase-8 activation. However, levels of CHOP and GRP78 remained unchanged after JMJD2B silencing., Conclusions: JMJD2B silencing induced CRC cell apoptosis via both mitochondria-related and death receptor-related pathways. The cleavage of Bid activated by caspase-8 might serve as a crosstalk mediator between these two pathways in CRC., (© 2014 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Wiley Publishing Asia Pty Ltd.)