These findings provide further indication that postdiagnosis aspirin therapy improved CRC overall survival, especially for patients with positive PTGS2 (COX-2) expression and mutated PIK3CA tumours.

Plenty of studies have assessed the association between intestinal metaplasia (IM) and gastric cancer risk, while the results were inconsistent. We aimed to assess the risk of gastric cancer among patients with IM. Systematic literature searches were conducted in PubMed, Embase and Cochrane databases. Baseline characteristics and outcomes from the included studies were extracted independently by two investigators. Either a fixed-effects or a random-effects model was used to composite the pooled OR for gastric cancer risk. Finally, a total of 21 studies, which comprised 402,636 participants and 4,535 gastric cancer patients, were finally included in the current meta-analysis. Compared with those participants without IM, IM patients were at a higher risk of gastric cancer (pooled OR = 3.58, 95% CI 2.71-4.73). We observed that incomplete IM (pooled OR = 9.48, 95% CI 4.33-20.78) but not complete IM (pooled OR = 1.55, 95% CI 0.91-2.65) was significantly associated with a higher gastric cancer risk. Besides, it appeared that gastric cancer risk was higher among patients with IM in the corpus (pooled OR = 7.39, 95% CI 4.94-11.06) than those with IM in the antrum only (pooled OR = 4.06, 95% CI 2.79-5.91). And the pooled ORs for gastric noncardia cancer and gastric cardia cancer were 4.98 (95% CI 3.12-7.95) and 1.93 (95% CI 1.15-3.24), respectively. In conclusion, patients with IM were at a higher risk of gastric cancer, especially for incomplete IM and IM in the corpus. The current evidence supports the use of IM subtypes in the surveillance of gastric cancer.

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Reported relationships among Helicobacter pylori infection, white blood cell (WBC) count and nonalcoholic fatty liver disease (NAFLD) are inconsistent and controversial. We, therefore, conducted a cross-sectional study to investigate the associations among the presence of NAFLD, WBC count and H pylori infection, as diagnosed using the 13C-urea breath test (UBT).This study included 20,389 subjects enrolled at the International Health Care Center of the Second Affiliated Hospital of the Zhejiang University School of Medicine from January 2015 to December 2015. All participants underwent a 13C-UBT for the diagnosis of H pylori infection and ultrasonography for NAFLD as well as a blood test to determine WBC count. Multivariate logistic regression was then performed to evaluate the relationship among H pylori infection, WBC count and NAFLD.H pylori infection was detected in 38.49% (7,848/20,389) of the subjects via the UBT, and NAFLD was present in 37.24% (7,592/20,389) of the subjects. The prevalence of H pylori infection was higher in the NAFLD group than in the control group (41.25% vs 36.85%, P <.001). Significant differences were found between various WBC quartiles and H pylori infection, age, gender, body mass index (BMI), systolic blood pressure (SBP), diastolic blood pressure (DBP), high-sensitivity C-reactive protein (HS-CRP), glycosylated hemoglobin (HbA1c), triglyceride (TG), low-density lipoprotein (LDL-C), fasting blood glucose (FPG), homeostasis model assessment of insulin resistance (HOMA-IR), and smoking. Multivariate logistic regression revealed that the combination of H pylori infection and WBC count (odds ratio [OR] = 1.067, 95% confidence interval [CI]: 1.014, 1.093; P = .007; OR = 1.165, 95% CI: 1.023, 1.488; P <.001; OR = 1.183, 95% CI: 1.085, 1.559; P <.001, respectively) was positively associated with NAFLD.H pylori infection and WBC count may contribute to the pathogenesis of NAFLD.

BackgroundZIC1, a vital transcription factor with zinc finger domains, has been implicated in the process of neural development. We previously showed that ZIC1 may function as a tumour suppressor in gastrointestinal cancers. However, the molecular mechanism underlying ZIC1 participation in tumour progression remains unknown.MethodsThe role of ZIC1 on cell proliferation and migration was examined. The regulation of sonic hedgehog (Shh), phosphoinositide 3-kinase (PI3K) and mitogen-activated protein kinase (MAPK) signaling pathways after ectopic expression of ZIC1 in gastric cancer cells were evaluated.ResultsOverexpression of ZIC1 contributes to the inhibition of cell proliferation migration and cell-cycle distribution in gastric cancer. The modulation of G1/S checkpoint by ZIC1 is mainly mediated through the regulation of cyclin-dependent kinases (p21 Waf1/Cip1, p27 Kip1 and cyclin D1). In addition, ZIC1 can inactivate the level of phospholated Akt and Erk1/2, and transcriptionally regulate sonic hedgehog (Shh) signaling, thus leading to regulate the expression of p21 Waf1/Cip1 and cyclin D1. Finally, we have systemically identified ZIC1 downstream targets by cDNA microarray analysis and revealed that 132 genes are down-regulated and 66 genes are up-regulated after transfection with ZIC1 in gastric cancer cells. These candidate genes play critical roles in cell proliferation, cell cycle and cell motility.ConclusionsOverexpression of ZIC1 results in inactivation of Shh, PI3K and MAPK signaling pathways, as well as regulation of multiple downstream targets which are essential for the development and progression of gastric cancer. ZIC1 serves as a potential therapeutic target for gastric cancer.

The objective of this research paper is to evaluate the effect of prophylactic nitroglycerin in the prevention of post-endoscopic retrograde cholangiopancreatography (ERCP) pancreatitis (PEP) by performing a meta-analysis of randomized controlled trials (RCTs). Electronic databases, including PubMed, EMBASE, the Cochrane library, and the Science Citation Index, were searched to retrieve relevant trials. Outcome measures were the incidence of PEP. Four RCTs, enrolling a total of 856 patients, were included. Meta-analysis of these trials indicated a significant association between the use of nitroglycerin and the reduction of PEP (RR 0.60; 95%CI: 0.39-0.92; P = 0.02). However, subsequent sensitive analysis failed to confirm that nitroglycerin was statistically superior to a placebo in reducing PEP (RR 0.68; 95%CI: 0.41-1.11; P = 0.12). Based on the limitations in this meta-analysis, prophylactic use of nitroglycerine for all patients who underwent ERCP is not recommended. Further clinical trials are required to confirm the effect of nitroglycerin in the prevention of PEP.

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Gastric cancer is one of the most common cancers and is a leading cause of mortality worldwide. 1,2 The National Central Cancer Registry of China (NCCR) estimated that there were 679 000 new cases, and more than 498 000 deaths from this disease in China in 2015. 3 There were an estimated 27 000 new cases and 11 140 deaths in the United States in 2019. 4,5 Gastric cancer is a heterogeneous disease, with significant differences in pathological features, biological behaviours and gene expression profiles. Despite advances in diagnosis and treatment, the disease tends to be prevalent in younger patients. The presence of late-stage clinical disease at the time of diagnosis indicates a high risk of recurrence and metastasis, along with poor prognosis. Therefore, elucidation of the molecular mechanisms involved in the tumorigenesis and disease progression of gastric cancer, with the goal of identifying potential biomarkers and therapeutic targets, is an unmet clinical need. The reprogramming of energy metabolism is an emerging hallmark of malignant tumours. 6 This new perspective suggests that malignant tumours are a metabolic disease. Fast-growing tumour