Overall, this meta-analysis finds no relation between n-3 PUFAs intake and risk of CRC. The observed subsite heterogeneity within colon cancer and the possible effect modification by latency time merit further studies.
BackgroundRunt-related transcription factor 3 (RUNX3) is a member of the runt-domain family of transcription factors and has been reported to be a candidate tumor suppressor in gastric cancer. However, the association between RUNX3 promoter methylation and gastric cancer remains unclear.MethodsWe systematically reviewed studies of RUNX3 promoter methylation and gastric cancer published in English or Chinese from January 2000 to January 2011, and quantified the association between RUNX3 promoter methylation and gastric cancer using meta-analysis methods.ResultsA total of 1740 samples in 974 participants from seventeen studies were included in the meta-analysis. A significant association was observed between RUNX3 promoter methylation and gastric cancer, with an aggregated odds ratio (OR) of 5.63 (95%CI 3.15, 10.07). There was obvious heterogeneity among studies. Subgroup analyses (including by tissue origin, country and age), meta-regression were performed to determine the source of the heterogeneity. Meta-regression showed that the trend in ORs was inversely correlated with age. No publication bias was detected. The ORs for RUNX3 methylation in well-differentiated vs undifferentiated gastric cancers, and in intestinal-type vs diffuse-type carcinomas were 0.59 (95%CI: 0.30, 1.16) and 2.62 (95%CI: 1.33, 5.14), respectively. There were no significant differences in RUNX3 methylation in cancer tissues in relation to age, gender, TNM stage, invasion of tumors into blood vessel or lymphatic ducts, or tumor stage.ConclusionsThis meta-analysis identified a strong association between methylation of the RUNX3 promoter and gastric cancer, confirming the role of RUNX3 as a tumor suppressor gene.
Background The essence of energy metabolism has spread to the field of esophageal cancer (ESC) cells. Herein, we tried to develop a prognostic prediction model for patients with ESC based on the expression profiles of energy metabolism associated genes. Materials and methods The overall survival (OS) predictive gene signature was developed, internally and externally validated based on ESC datasets including The Cancer Genome Atlas (TCGA), GSE54993 and GSE19417 datasets. Hub genes were identified in each energy metabolism related molecular subtypes by weighted gene correlation network analysis, and then enrolled for determination of prognostic genes. Univariate, LASSO and multivariate Cox regression analysis were applied to assess prognostic genes and build the prognostic gene signature. Kaplan-Meier curve, time-dependent receiver operating characteristic (ROC) curve, nomogram, decision curve analysis (DCA), and restricted mean survival time (EMST) were used to assess the performance of the gene signature. Results A novel energy metabolism based eight-gene signature (including UBE2Z, AMTN, AK1, CDCA4, TLE1, FXN, ZBTB6 and APLN) was established, which could dichotomize patients with significantly different OS in ESC. The eight-gene signature demonstrated independent prognostication potential in patient with ESC. The prognostic nomogram constructed based on the gene signature showed excellent predictive performance, whose robustness and clinical usability were higher than three previous reported prognostic gene signatures. Conclusions Our study established a novel energy metabolism based eight-gene signature and nomogram to predict the OS of ESC, which may help in precise clinical management.
Rationale:Bleeding in the gastrointestinal tract is a common complication of oral anticoagulant therapy (AT), and it usually appears as mucosal erosion or ulcer; however, intestinal submucosal hematoma (ISH) is an uncommon cause of hemorrhage.Patient concerns:This report presents the case of a 70-year-old woman with acute hematochezia induced by AT. She underwent computed tomography and endoscopy.Diagnoses:Colon submucosal hematoma.Interventions:Conservative treatment had no effect, and the patient underwent emergency surgery.Outcomes:Surgical resection showed hemorrhage and necrosis in the left colon, and the patient recovered 24 hours after surgery and continued AT.Lessons:The present case indicates that the ISH should be kept in mind as a complication of AT. It can be managed conservatively in some stable patients, but emergency surgery may be needed in some serious situations.
SummaryBackgroundPost-polypectomy hemorrhage is one of the complications of colonscopic polypectomy. And there is no definitive and convenient laboratory test that could be used to predict risk of delayed post-polypectomy hemorrhage. This research aimed to study risk prediction of delayed post-polypectomy hemorrhage using serum C-reactive protein (CRP) level as a marker.Material/MethodsIn a retrospective, case-controlled study, 302 cases of post-polypectomy patients were divided into hemorrhage group and non-hemorrhage group. The CRP levels 24-hours after colonscopic treatment were compared between the two groups to assess whether elevated serum CRP levels in addition to other risk factors such as age, gender, smoking, alcohol consumption, hypertension (AHT) and size of polyps may predict risk of delayed post-polypectomy hemorrhage.ResultsThe hemorrhage group had significantly higher levels of serum CRP (32.50±17.34 mg/L vs. 6. 32±6.02 mg/dL) and were also having a higher incidence of hypertension compared to the non- hemorrhage group (both P<0.05). Patients with elevated serum CRP levels (≥10mg/L) after colonscopic treatment are at a higher risk of developing post-polypectomy hemorrhage (OR 1.329, 95%CI 1.125–1.571) as compared with patients whose CRP levels were not increased.ConclusionsA higher level of serum CRP may serve as an indicator of delayed post-polypectomy hemorrhage and there appears to be a direct relationship between the serum CRP levels and the risk of post-polypectomy hemorrhage: the higher CRP levels the higher the risk of post-polypectomy hemorrhage.
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