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Background Colon cancer is a worldwide leading cause of cancer-related mortality, and the prognosis of colon cancer is still needed to be improved. This study aimed to construct a prognostic model for predicting the prognosis of colon cancer. Methods The gene expression profile data of colon cancer were obtained from the TCGA, GSE44861, and GSE44076 datasets. The WGCNA module genes and common differentially expressed genes (DEGs) were used to screen out the prognosis-associated DEGs, which were used to construct a prognostic model. The performance of the prognostic model was assessed and validated in the TCGA training and microarray validation sets (GSE38832 and GSE17538). At last, the model and prognosis-associated clinical factors were used for the construction of the nomogram. Results Five colon cancer-related WGCNA modules (including 1160 genes) and 1153 DEGs between tumor and normal tissues were identified, inclusive of 556 overlapping DEGs. Stepwise Cox regression analyses identified there were 14 prognosis-associated DEGs, of which 12 DEGs were included in the optimized prognostic gene signature. This prognostic model presented a high forecast ability for the prognosis of colon cancer both in the TCGA training dataset and the validation datasets (GSE38832 and GSE17538; AUC > 0.8). In addition, patients’ age, T classification, recurrence status, and prognostic risk score were associated with the prognosis of TCGA patients with colon cancer. The nomogram was constructed using the above factors, and the predictive 3- and 5-year survival probabilities had high compliance with the actual survival proportions. Conclusions The 12-gene signature prognostic model had a high predictive ability for the prognosis of colon cancer.

Changes in dietary vitamin C intake have been related to the risks of various cancers. However, the association between dietary vitamin C intake and the risk of ovarian cancer has not been fully determined. A meta-analysis was performed to evaluate the relationship between vitamin C intake and ovarian cancer risk. Observational studies that evaluated the association between vitamin C intake and ovarian cancer risk were identified via systematic search of PubMed and Embase databases. A random effect model was used to combine relative risk (RR) with corresponding 95% confidence intervals (CI). As a result, 16 studies (5 cohort studies and 11 case-control studies) with 4,553 cases and 439,741 participants were included. Pooled results showed that dietary vitamin C intake had non-significant association on the risk of ovarian cancer (RR=0.95, 95%CI= 0.81-1.11, I2= 52.1%, Pfor heterogeneity= 0.008). Subgroup analyses according to characteristics including geographic location and study design showed consistent results with the overall result. In summary, findings from this study indicated that dietary vitamin C intake is not associated with the risk of ovarian cancer.

BackgroundIn China, the prevalence and mortality of colorectal cancer (CRC) have always been high, and more than 95% of CRC cases have evolved from colorectal polyps (CPs), especially adenoma. Early detection and treatment of CPs through colonoscopy is essential to reduce the incidence of CRC. Helicobacter pylori (Hp) is regarded as a risk factor for gastritis and gastric cancer and may also be a risk factor for CPs and CRC. However, few studies based on vast clinical cases exist in China to clarify whether Hp is a risk factor for CPs and CRC, and whether Hp-positive patients need to undergo colonoscopy checks earlier. This article attempts to make up for that deficiency.MethodThis cross-sectional study was conducted based on 13,037 patients without a treatment history of Hp who underwent their first gastroscopy and colonoscopy simultaneously at The First Affiliated Hospital of Zhejiang Chinese Medical University from January 2018 to December 2019. Pearson χ2 test and logistic regression were used to determine whether Hp is a risk factor for CPs and CRC. Multifactor analysis of variance was used to define the impact of Hp on CPs prevalence with different ages, sexes.ResultsFor Chinese individuals, Hp is a risk factor for CPs and CRC. The odds ratio (OR) value are 1.228 (95% CI, 1.130 to 1.336) and 1.862 (95% CI 1.240-2.796), respectively. Hp-positive patients have a higher probability of multiple or large intestinal polyps. However, Hp infection does not increase the incidence of adenomas, nor does it affect the pathological type of adenomas. The OR of Hp on the risk of CPs was 1.432 (95%CI 1.275-1.608) for males but increased to 1.937 (95%CI 1.334-2.815) for those aged 35 to 40. For females, the results were similar.ConclusionsFor the Chinese, Hp is a risk factor for CPs and CRC (OR>1); the infection of Hp increased CPs risk in Chinese of all ages, especially aged 35-40, suggesting that Hp-positive patients should undergo colonoscopy frequently.

Shenqi pill (SQP), a famous traditional Chinese medicine (TCM) herbal formula derived from Jinguiyaolue (Synopsis of Prescriptions of the Golden Chamber), has long been used to treat kidney yang deficiency syndrome. According to the TCM treatment principle that the liver and kidney are homologies, the clinical use of SQP in the treatment of nonalcoholic steatohepatitis (NASH) has achieved a good effect. However, the active targeted genes and underlying mechanism remain unclear. In this study, we aimed to explore the treatment mechanism of SQP in NASH rats, which may further contribute to the in-depth exploration of SQP in clinical applications. Network pharmacology analysis was used to screen the target genes of SQP for NASH treatment based on public databases. Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis, and protein–protein interaction (PPI) analysis were used to search for crucial target genes and mechanisms. UPLC–MS/MS was used to verify the active compounds of the SQP screened. The hepatic pathology and biochemical indicators of rats were used to judge the modeling results and the curative effect of SQP. Western blotting and qRT–PCR were used to verify the expression of crucial target genes at the protein and RNA levels, respectively. Network pharmacology analysis and bioinformatics analysis showed that PTGS2, JUN, MYC, and CDKN1A might be crucial target genes in the primary mechanism of SQP in treating NASH and improving the inflammatory response. The UPLC–MS/MS results confirmed that the hub active compound, quercetin, screened out through the TCMSP database, is indeed present in SQP. Hepatic injury and lipid metabolism indicators of NASH rats were significantly improved after SQP treatment. The results of WB and qRT–PCR showed that the expression of PTGS2, JUN, MYC, and CDKN1A was higher in NASH rats than in normal rats and decreased after SQP treatment. The expression of inflammatory cytokines (IL-1β, IL-6, TNF-α) was reduced after SQP treatment, which confirmed that SQP could improve hepatic inflammation in rats. These results suggested that SQP could ameliorate NASH in rats, and that quercetin may be the critical active compound that exerts the therapeutic effect.