Transfer RNA modifications have emerged as critical regulators of translational reprogramming, yet their roles in colorectal cancer (CRC) remain largely elusive. Here, we find that tRNA N1-methyladenosine (m1A) methyltransferase TRMT6 is upregulated in human CRC tissues and high TRMT6 expression correlates with poor survival in patients with CRC. Using orthotopic, metastatic and conditional knockout mouse models, we establish the oncogenic role of TRMT6 in CRC. Mechanistically, TRMT6 increases tRNA m1A levels by maintaining the stability of the TRMT6–TRMT61A complex. Targeting TRMT6-mediated tRNA m1A modification in CRC cells destabilizes tRNA-Lys-TTT-1-1 and impairs histone mRNA translation in a codon-biased manner, thereby restricting histone synthesis and hindering cell cycle progression. Our study provides evidence that TRMT6 functions as a translational checkpoint in the accelerated histone synthesis of CRC cells, highlighting TRMT6 as a promising target for potential anti-CRC therapies. Tao et al. study the role of TRMT6 in colorectal cancer, where it is upregulated and show that TRMT6 supports histone biosynthesis by stabilizing tRNA-Lys-TTT-1-1. Targeting TRMT6 reduced histone mRNA translation in a codon-biased manner.

Berberine has been reported as a safe and effective pharmacological agent to reduce colorectal adenoma recurrence after polypectomy. This retrospective cohort study is an extended follow-up of a previous clinical trial (NCT02226185) during the post-treatment observational phase. We aim to evaluate the long-term protective effects of berberine on adenoma recurrence. Among 895 patients who finished the previous 2-year randomized trial, we recruited 781 patients at 7 clinical centers across 6 provinces in China. The primary outcome is adenoma recurrence. Between December 29, 2018, and October 10, 2024, 648 patients underwent at least one colonoscopy during the follow-up. The protective effects of berberine persist for at least 6 years after treatment cessation, with lower adenoma recurrence rate (34.7% vs. 52.1%) and lower neoplasm occurrence rate (63.4% vs. 71.0%). Berberine may serve as a potential long-term preventive agent against adenoma recurrence after polypectomy.

Colorectal cancer (CRC) is a leading cause of cancer deaths worldwide and in recent years its incidence is increasing rapidly in China, which constitutes a major public health burden. Almost 90% of CRC cases develop from precursor adenomatous polyps, through a series of genetic changes known as adenoma-carcinoma sequence during at least 10 years. Detection and removal of colorectal adenoma (CRA) could reduce CRC mortality risk by colonoscopy, but the recurrence rate is high. Our previous RCT study (NCT02226185) found that oral Berberine (BBR), a natural isoquinoline alkaloid extracted from the Chinese herb Coptis chinensis for 2 years significantly reduced recurrence after endoscopic removal of CRA (RR 0.77, 95% CI 0.66-0.91; p=0.001). The study recruited 895 participants who had undergone complete polypectomy within 6 months in seven hospital centers across six provinces in China between Nov 14, 2014, and Dec 30, 2016. Participants were randomly assigned (1:1) to receive BBR (0·3 g twice daily) or placebo tablets via block randomization for 2 years. After the end of randomized treatment, we continued this Follow-up Study to track adenoma recurrence for an average of 6 years till Sep 30, 2024. Besides 114 participants lost to follow up, we obtained follow-up information for 781 participants, 648 of whom underwent at least one colonoscopy after the end of study treatment and were included in this analysis. Mantel-Haenszel test was used to compute relative risks (RRs) and 95% confidence intervals (CIs) for the effect of BBR on risk of adenoma recurrence. Cox proportional-hazards model and Andersen-Gill model were used to analyze multi-recurrence by time. The study is registered with ClinicalTrials.gov, number NCT06629051. During the average 6 years follow up, we found that participants in the BBR group still had a substantially and statistically significantly lower risk of CRA than those in the placebo group (34.7% versus 52.1%; adjusted RR = 0.639, 95% CI = 0.508 to 0.785, P<0.001) and a reduction in risk of any neoplasm including inflammatory polyps, serrated lesions and colorectal cancer (adjusted RR = 0.874, 95% CI = 0.775 to 0.983, P = 0.022). Meanwhile the risk of non-advanced CRA in BBR group was lower than that in placebo group (adjusted RR = 0.634, 95% CI = 0.497 to 0.790, P<0.001). The incidence of adenoma recurrence was significantly lower in participants receiving BBR (HR= 0.601; 95% CI = 0.473-0.765; P<0.001). And in every year after treatment ended, the risk of adenoma recurrence in BBR group was lower than placebo group for all RRs<1.0 but some of which were not statistically significant. Generally, the protective effect of berberine on risk of colorectal recurrence extends up to 6 years after cessation of active treatment, even in the absence of continued supplementation.

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.

BACKGROUND:Colorectal carcinogenesis and progression are related to the gut microbiota and the tumor immune microenvironment. Our previous clinical trial demonstrated that berberine (BBR) hydrochloride might reduce the recurrence and canceration of colorectal adenoma (CRA). The present study aimed to further explore the mechanism of BBR in preventing colorectal cancer (CRC). METHODS:We performed metagenomics sequencing on fecal specimens obtained from the BBR intervention trial, and the differential bacteria before and after medication were validated using quantitative polymerase chain reaction. We further performed ApcMin/+ animal intervention tests, RNA sequencing, flow cytometry, immunohistochemistry, and enzyme-linked immunosorbent assays. RESULTS:The abundance of fecal Veillonella parvula ( V . parvula ) decreased significantly after BBR administration ( P = 0.0016) and increased through the development from CRA to CRC. Patients with CRC with a higher V. parvula abundance had worse tumor staging and a higher lymph node metastasis rate. The intestinal immune pathway of Immunoglobulin A production was activated, and the expression of TNFSF13B (Tumor necrosis factor superfamily 13b, encoding B lymphocyte stimulator [BLyS]), the representative gene of this pathway, and the genes encoding its receptors (interleukin-10 and transforming growth factor beta) were significantly upregulated. Animal experiments revealed that V. parvula promoted colorectal carcinogenesis and increased BLyS levels, while BBR reversed this effect. CONCLUSION:BBR might inhibit V. parvula and further weaken the immunomodulatory effect of B cells induced by V. parvula , thereby blocking the development of colorectal tumors. TRIAL REGISTRAION:ClinicalTrials.gov, No. NCT02226185.

BackgroundSerrate d polyps (SP) is associated with an increased risk of colorectal cancer. Patients with SP history tend to have SP recurrence. However, the risk factors for metachronous polyps (MP) in those patients are not well established. MethodsData of colonoscopy were retrospectively reviewed from October 2012 to October 2021. The pathology database, electronic medical records and telephone follow-up data were also observed. ResultsA total of 906 patients were studied including 278 patients with MPs and 628 patients without. The multiplicity of polyps (OR, 13.63; 95% CI, 8.80-21.75), older age (OR, 5.71; 95% CI, 1.87-20.63), abdominal obesity (OR, 2.46; 95% CI, 0.98-6.42), current smoker (OR, 2.93; 95% CI, 1.15-7.83) and sedentary lifestyle (OR, 1.41; 95% CI, 1.22-1.65) are significantly associated with the risk of MPs. Patients with baseline SP < 10 mm were more likely to develop higher or same risk-grade polyps (HSRGP) (P = 0.0014). Patients with non-clinically significant SPs whether coexisted with adenoma or not were more likely to develop HSRGPs when compared to others (P < 0.001). ConclusionTotal number of polyps, older age, sedentary behavior, abdominal obesity and smoking status contributed to the risk of MPs at surveillance colonoscopy. Patients with grade 1 SPs might require closer surveillance. SPs coexisting with conventional adenoma did not increase the risk of MPs but may increase the risk of developing HSRGPs.

Transfer RNA (tRNA) plays a central role in translation by functioning as a biological link between messenger RNA (mRNA) and proteins. One prominent feature of the tRNA molecule is its heavily modified status, which greatly affects its biogenesis and function. Modifications within the anticodon loop are crucial for translation efficiency and accuracy, whereas other modifications in the body region affect tRNA structure and stability. Recent research has revealed that these diverse modifications are critical regulators of gene expression. They are involved in many important physiological and pathological processes, including cancers. In this review we focus on six different tRNA modifications to delineate their functions and mechanisms in tumorigenesis and tumor progression, providing insights into their clinical potential as biomarkers and therapeutic targets.

In our previous study, we reported that sirtuin5 (SIRT5), a member of the NAD(+)-dependent class III histone deacetylase family, is highly expressed in colorectal cancer (CRC). Herein we show that SIRT5 knockdown impairs the production of ribose-5-phosphate, which is essential for nucleotide synthesis, resulting in continuous and irreparable DNA damage and consequently leading to cell cycle arrest and enhanced apoptosis in CRC cells. These SIRT5 silencing-induced effects can be reversed by nucleoside supplementation. Mechanistically, SIRT5 activates transketolase (TKT), a key enzyme in the non-oxidative pentose phosphate pathway, in a demalonylation-dependent manner. Furthermore, TKT is essential for SIRT5-induced malignant phenotypes of CRC both in vivo and in vitro. Altogether, SIRT5 silencing induces DNA damage in CRC via post-translational modifications and inhibits tumor growth, suggesting that SIRT5 can serve as a promising target for CRC treatment.

Background Currently, tRNA-derived small RNAs (tsRNAs) are recognized as a novel and potential type of non-coding RNAs (ncRNAs), which participate in various cellular processes and play an essential role in cancer progression. However, tsRNAs involvement in colorectal cancer (CRC) progression remains unclear. Methods Sequencing analyses were performed to explore the tsRNAs with differential expression in CRC. Gain- and loss-of functions of 5’tiRNA-His-GTG were performed in CRC cells and xenograft tumor to discover its role in the progression of CRC. Hypoxia culture and hypoxia inducible factor 1 subunit alpha (HIF1α) inhibitors were performed to uncover the biogenesis of 5’tiRNA-His-GTG. The regulation of 5’tiRNA-His-GTG for large tumor suppressor kinase 2 (LATS2) were identified by luciferase reporter assay, western blot, and rescue experiments. Results Here, our study uncovered the profile of tsRNAs in human CRC tissues and confirmed a specific tRNA half, 5’tiRNA-His-GTG, is upregulated in CRC tissues. Then, in vitro and in vivo experiments revealed the oncogenic role of 5’tiRNA-His-GTG in CRC and found that targeting 5’tiRNA-His-GTG can induce cell apoptosis. Mechanistically, the generation of 5’tiRNA-His-GTG seems to be a responsive process of tumor hypoxic microenvironment, and it is regulated via the HIF1α/angiogenin (ANG) axis. Remarkably, LATS2 was found to be an important and major target of 5’tiRNA-His-GTG, which renders 5’tiRNA-His-GTG to “turn off” hippo signaling pathway and finally promotes the expression of pro-proliferation and anti-apoptosis related genes. Conclusions In summary, the findings revealed a specific 5’tiRNA-His-GTG-engaged pathway in CRC progression and provided clues to design a novel therapeutic target in CRC.

A previous study by our research group showed that sirtuin5 (SIRT5), a member of the class III NAD＋-dependent deacetylase family, is highly expressed in colorectal cancer (CRC). The present study showed that deletion of SIRT5 induced cell cycle arrest and apoptosis as a result of continuous and irreparable DNA damage in CRC cells, a consequence of the impaired production of ribose-5-phosphate (R5P) which is essential for nucleotide synthesis. Consistently, the cell cycle arrest and apoptosis induced by SIRT5 silencing could be reversed by supplementation with four nucleotides. Moreover, metabolic profiling revealed that silencing of SIRT5 could inhibit the non-oxidative pentose phosphate pathway (PPP), which produces R5P, required for base ribosylation. Notably, SIRT5 activates transketolase (TKT), the key enzyme in the cellular non-oxidative PPP, by mediating its lysine demalonylation through the interaction between SIRT5 and TKT. Furthermore, the results demonstrated that TKT is essential for the SIRT5-induced malignant phenotypes of CRC, both in vivo and in vitro. These results therefore revealed that the increased lysine malonylation levels of TKT caused by silencing SIRT5 suppresses non-oxidative pentose phosphate metabolism, leading to a low-nucleotide pool. This in turn induces DNA damage in tumor cells and inhibits proliferation, suggesting that SIRT5 may serve as a potential anticancer target.

Objective Up to now, non-invasive diagnosis of laterally spreading tumor (LST) and prediction of adenoma recurrence after endoscopic resection of LSTs is inevitable. This study aimed to identify a microbial signature with clinical significance of diagnosing LSTs and predicting adenoma recurrence after LSTs colectomy. Methods We performed 16S rRNA sequencing in 24 mucosal samples, including 5 healthy controls (HC), 8 colorectal adenoma (CRA) patients, and 11 LST patients. The differentiating microbiota in fecal samples was quantified by qPCR in 475 cases with 113 HC, 208 CRA patients, 109 LST patients, and 45 colorectal cancer (CRC) patients. We identified differentially abundant taxa among cases and controls using linear discriminant analysis effect size analysis. ROC curve was used to evaluate diagnostic values of the bacterial candidates. Pairwise comparison of AUCs was performed by using the Delong’s test. The Mantel-Haenszel hazard models were performed to determine the effects of microbial compositions on recurrence free survival. Results The microbial dysbiosis of LST was characterized by relative high abundance of the genus Lactobacillus-Streptococcus and the species enterotoxigenic Bacteroides fragilis (ETBF)–Peptostreptococcus stomatis (P. stomatis)–Parvimonas micra (P. micra). The abundance of ETBF, P. stomatis, and P. micra were steadily increasing in LST and CRC groups. P. stomatis behaved stronger value on diagnosing LST than the other two bacteria (AUC 0.887, 95% CI 0.842–0.931). The combination of P. stomatis, P. micra, and ETBF (AUC 0.922, 95% CI 0.887–0.958) revealed strongest diagnostic power with 88.7% sensitivity and 81.4% specificity. ETBF, P. stomatis, and P. micra were associated with malignant LST (PP.stomatis = 0.0015, PP.micra = 0.0255, PETBF = 0.0169) and the abundance of IL-6. The high abundance of P. stomatis was related to the adenoma recurrence after LST resection (HR = 3.88, P = 0.008). Conclusions Fecal microbiome signature (ETBF–P. stomatis–P. micra) can diagnose LSTs with high accuracy. ETBF, P. stomatis, and P. micra were related to malignant LST and P. stomatis exhibited high predictive value on the adenoma recurrence after resection of LSTs. The fecal microbiome signature of LST may provide a noninvasive alternative to early detect LST and predict the adenoma recurrence risk after resections of LSTs.

IgG4-related disease (IgG4-RD) is an immune-mediated fibroinflammatory disease that responds to glucocorticoids, which is gradually well known in recent years. It can involve multiple organs of patients, including pancreas, bile duct, gallbladder, salivary gland, orbital tissue, lung, liver, lacrimal gland, kidney, retroperitoneal, aorta, thyroid and lymph node, [1] in which gastrointestinal involvement is relatively rare [2]. Most of the known reports of isolated gastric IgG4-related lesions were accidental found (in physical examination or other site examination), and often treated as Gastrointestinal Stromal Tumors (GIST) lead to surgically resection. In addition, Calcified Fibrous Tumor (CFT) in gastrointestinal tract often occurs with submucosa [3] is histologically similar to IgG4-RD, [4] whether it belongs to IgG4-RD is still controversial.

ObjectiveSerrated 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.MethodsThe 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.ResultsThe 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.ConclusionLarge SP and SSL with high‐grade intraepithelial neoplasia are associated with synchronous advanced neoplasia and require timely surveillance.

Rationale: Post-translational modifications have emerged as vital players in alterations to tumor metabolism, including amino acid metabolic reprogramming. Jumonji domain-containing protein 2B (JMJD2B) enhances colorectal cancer (CRC) cell survival upon glucose deficiency. In the present study, we hypothesized that JMJD2B affects tumor cell amino acid metabolism in CRC and consequently promotes survival of CRC cells upon glucose deprivation. Methods: Non-target metabolic profiling was used to evaluate the roles of JMJD2B in CRC cell metabolism under glucose starvation. The roles of amino acid alterations induced by JMJD2B on CRC cell survival were determined by cell viability, immunoblotting, and clonogenic assays, and flow cytometry. The underlying mechanisms by which JMJD2B affected CRC cell metabolism were assessed using immunofluorescence staining, chromatin immunoprecipitation assays, electron microscopy in CRC cell lines, and using xenograft models. The correlation between JMJD2B and LC3B expression in human CRC specimens was assessed using immunohistochemistry. Results: Profound metabolic reprogramming was detected in JMJD2B knockdown CRC cells under glucose deficiency, especially those involving amino acid metabolites. Silencing of JMJD2B reduced the levels of certain amino acids that were induced by glucose deficiency. Among these amino acids, asparagine (Asn), phenylalanine (Phe), and histidine (His) promoted CRC cell survival under glucose starvation when JMJD2B was knocked down. Mechanistically, downregulation of JMJD2B inhibited autophagy in CRC cells through epigenetic regulation of microtubule associated protein 1 light chain 3 beta (LC3B), and subsequently decreased intracellular amino acid (Asn, Phe, His) levels under glucose deprivation, thus suppressing the survival of CRC cells. Using a nude mouse xenograft model, we verified that inhibiting JMJD2B could decrease the levels of amino acids (Asn, Phe, His). In addition, the inhibitory effects of JMJD2B-knockdown on tumor growth and amino acids level were rescued by overexpression of LC3B. Furthermore, we observed that the high expression of LC3B was more likely detected in tissuses with high expression of JMJD2B (P < 0.001) in 60 human CRC tissues. Conclusion: These results indicated that JMJD2B sustained the intracellular amino acids derived from autophagy in CRC cells upon glucose deficiency, partly through epigenetic regulation of LC3B, thus driving the malignancy of CRC.

Background. The coexistence of colorectal polyps with laterally spreading tumors (LSTs) is commonly observed during colonoscopy. However, there are rare studies that assess the malignant risks for LSTs with colorectal polyps, which might largely contribute to further strategies of treatment and follow-up plans in LSTs. Methods. We conducted a retrospective cohort study that enrolled 206 patients with LSTs in the Endoscopy Center and Endoscopy Research Institute, Renji Hospital, Shanghai Jiao Tong University, China. The subjects with LSTs were divided into two groups: the nonpolyp group with 89 patients and the polyp group with 117 patients. Binary logistic regression was used to identify the independent predictors of outcomes of interest. Results. The risk of the polyps’ coexistence phenomenon increased in males compared with females (OR=2.138, p=0.047), especially in those between 50 and 75 years old (OR=7.074, p=0.036). Tumor size (3–4 cm), LSTs with tubulovillous types, and history of polyps statistically increased the risk of the polyp coexistence phenomenon (OR=5.768, p=0.003; OR=36.345, p=0.024; OR=13.245, p<0.0001, respectively). LST-NG-PD (OR=20.982, p=0.017) and LSTs≥5 cm (OR=37.604, p=0.038) notably increased the malignant risk of LSTs. When the simultaneous polyps are located in the right colon, the risk of malignant LSTs (OR=58.540, p=0.013) positively increased. Conclusion. The simultaneous colorectal polyps in the right colon were the most important risk factor to predict the malignant risk of LSTs.

The enrichment of Enterotoxigenic Bacteroides fragilis (ETBF) has been identified in CRC patients and associated with worse prognosis. Cancer stem cells (CSCs) play essential roles in CRC development. However, whether ETBF is involved in CSCs regulation is unknown. To clarify the role of ETBF in CSCs properties, we performed extreme limited dilution assays (ELDA) in nude mice injected with ETBF-treated or untreated CRC cells subcutaneously, tumor organoids culture in azoxymethane (AOM) mouse model after gavaging with or without ETBF, and cell sphere formation assay after incubating CRC cell lines with or without ETBF. The results indicated that ETBF increased the stemness of CRC cells in vivo and in vitro. Furthermore, ETBF enhanced the expression of core stemness transcription factors Nanog homeobox (NANOG) and sex determining region Y-box 2 (SOX2). Histone H3 Lysine 9 trimethylation (H3K9me3) is critical in regulating CSCs properties. As an epigenetic and transcriptional regulator, JmjC-domain containing histone demethylase 2B (JMJD2B) is essential for embryonic stem cell (ESC) transformation and H3K9me3 demethylation. Mechanistically, ETBF infection significantly upregulated JMJD2B levels in CRC cell lines and nude mice xenograft model. JMJD2B epigenetically upregulated NANOG expression via demethylating its promoter H3K9me3, to mediate ETBF-induced stemness of CRC cells. Subsequently, we found that the Toll-like receptor 4 (TLR4) pathway, activated by ETBF, contributed to the enhanced expression of JMJD2B via nuclear transcription factor nuclear factor of activated T cells 5 (NFAT5). Finally, in human CRC samples, the amount of ETBF positively correlated with nuclear NFAT5, JMJD2B, and NANOG expression levels. In summary, ETBF upregulated JMJD2B levels in a TLR4-NFAT5-dependent pathway, and played an important role in stemness regulation, which promoted colorectal carcinogenesis.

传统学习模式不利于临床教学质量的提高,不利于学生实践能力、自学能力和沟通能力的发展.介绍以团队为基础的学习(TBL)在国内外临床教学中的应用,并分析其可行性和利弊,全面介绍TBL的教学过程、分组管理和评价反馈体系,并提出国内开展TBL遇到的难点及未来展望.TBL注重理论与实践,个人与团队,竞争与合作,自主性与协作性的融合,是对传统学习模式的优化和完善,在临床教学中,具有强大的应用前景.国内临床医学院在开展TBL时,需根据实际情况,扬长避短,在教学实践中进一步的探索适合国内的TBL模式,满足现代临床医学发展的需求.

Journal of Digestive DiseasesVolume 21, Issue 3 p. 125-126 EDITORIAL 2019 Novel coronavirus infection and gastrointestinal tract Correction(s) for this article Corrigendum Volume 21Issue 10Journal of Digestive Diseases pages: 600-600 First Published online: October 13, 2020 Qin Yan Gao, Qin Yan Gao orcid.org/0000-0001-9422-300X Division of Gastroenterology and Hepatology, Key Laboratory of Gastroenterology & Hepatology, Ministry of Health, State Key Laboratory of Oncogene and Related Genes, Shanghai Institute of Digestive Disease, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, ChinaSearch for more papers by this authorYing Xuan Chen, Ying Xuan Chen orcid.org/0000-0002-1883-7736 Division of Gastroenterology and Hepatology, Key Laboratory of Gastroenterology & Hepatology, Ministry of Health, State Key Laboratory of Oncogene and Related Genes, Shanghai Institute of Digestive Disease, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, ChinaSearch for more papers by this authorJing Yuan Fang, Corresponding Author Jing Yuan Fang [email protected] orcid.org/0000-0003-2282-0248 Division of Gastroenterology and Hepatology, Key Laboratory of Gastroenterology & Hepatology, Ministry of Health, State Key Laboratory of Oncogene and Related Genes, Shanghai Institute of Digestive Disease, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China Correspondence Jing Yuan Fang, Division of Gastroenterology and Hepatology, Key Laboratory of Gastroenterology & Hepatology, Ministry of Health, State Key Laboratory of Oncogene and Related Genes, Shanghai Institute of Digestive Disease, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, 145 Middle Shandong Road, Shanghai 200001, China. Email: [email protected]Search for more papers by this author Qin Yan Gao, Qin Yan Gao orcid.org/0000-0001-9422-300X Division of Gastroenterology and Hepatology, Key Laboratory of Gastroenterology & Hepatology, Ministry of Health, State Key Laboratory of Oncogene and Related Genes, Shanghai Institute of Digestive Disease, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, ChinaSearch for more papers by this authorYing Xuan Chen, Ying Xuan Chen orcid.org/0000-0002-1883-7736 Division of Gastroenterology and Hepatology, Key Laboratory of Gastroenterology & Hepatology, Ministry of Health, State Key Laboratory of Oncogene and Related Genes, Shanghai Institute of Digestive Disease, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, ChinaSearch for more papers by this authorJing Yuan Fang, Corresponding Author Jing Yuan Fang [email protected] orcid.org/0000-0003-2282-0248 Division of Gastroenterology and Hepatology, Key Laboratory of Gastroenterology & Hepatology, Ministry of Health, State Key Laboratory of Oncogene and Related Genes, Shanghai Institute of Digestive Disease, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China Correspondence Jing Yuan Fang, Division of Gastroenterology and Hepatology, Key Laboratory of Gastroenterology & Hepatology, Ministry of Health, State Key Laboratory of Oncogene and Related Genes, Shanghai Institute of Digestive Disease, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, 145 Middle Shandong Road, Shanghai 200001, China. Email: [email protected]Search for more papers by this author First published: 25 February 2020 https://doi.org/10.1111/1751-2980.12851Citations: 265Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat No abstract is available for this article. 1 CONFLICT OF INTEREST None. REFERENCES 1Wu F, Zhao S, Yu B, et al. A new coronavirus associated with human respiratory disease in China [published online ahead of print February 3, 2020]. Nature. https://doi.org/10.1038/s41586-020-2008-3. 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