Comprehensive analysis reveals key genes and environmental toxin exposures underlying treatment response in ulcerative colitis based on in-silico analysis and Mendelian randomization.

BACKGROUND: UC is increasingly prevalent worldwide and represents a significant global disease burden. Although medical therapeutics are employed, they often fall short of being optimal, leaving patients struggling with treatment non-responsiveness and many related complications. MATERIALS AND METHODS: The study utilized gene microarray data and clinical information from GEO. Gene enrichment and differential expression analyses were conducted using Metascape and Limma, respectively. Lasso Regression Algorithm was constructed using glmnet and heat maps were generated using pheatmap. ROC curves were used to assess diagnostic parameter capability, while XSum was employed to screen for small-molecule drugs exacerbating UC. Molecular docking was carried out using Autodock Vina. The study also performed Mendelian randomization analysis based on TwoSampleMR and used CTD to investigate the relationship between exposure to environmental chemical toxicants and UC therapy responsiveness. RESULTS: Six genes (ELL2, DAPP1, SAMD9L, CD38, IGSF6, and LYN) were found to be significantly overexpressed in UC patient samples that did not respond to multiple therapies. Lasso analysis identified ELL2 and DAPP1 as key genes influencing UC treatment response. Both genes accurately predicted intestinal inflammation in UC and impacted the immunological infiltration status. Clofibrate showed therapeutic potential for UC by binding to ELL2 and DAPP1 proteins. The study also reviews environmental toxins and drug exposures that could impact UC progression. CONCLUSIONS: We used microarray technology to identify DAPP1 and ELL2 as key genes that impact UC treatment response and inflammatory progression. Clofibrate was identified as a promising UC treatment. Our review also highlights the impact of environmental toxins on UC treatment response, providing valuable insights for personalized clinical management.

Comparison of clinical and pathological features between early-stage gastric-type and intestinal-type differentiated adenocarcinoma: a retrospective study.

BACKGROUND: The clinicopathological features and endoscopic characteristics under magnifying endoscopy with narrow band imaging (ME-NBI) between early-stage gastric-type differentiated adenocarcinoma (GDA) and intestinal-type differentiated adenocarcinoma (IDA) remain controversial. METHODS: Early gastric adenocarcinomas that underwent endoscopic submucosal dissection (ESD) in Nanjing Drum Tower Hospital between August 2017 and August 2021 were included in the present study. GDA cases and IDA cases were selected based on morphology and immunohistochemistry staining of CD10, MUC2, MUC5AC, and MUC6. Clinicopathological data and endoscopic findings in ME-NBI were compared between GDAs and IDAs. RESULTS: The mucin phenotypes of 657 gastric cancers were gastric (n = 307), intestinal (n = 109), mixed (n = 181) and unclassified (n = 60). No significant difference was observed in terms of gender, age, tumor size, gross type, tumor location, background mucosa, lymphatic invasion, and vascular invasion between patients with GDA and IDA. GDA cases were associated with deeper invasion than IDA cases (p = 0.007). In ME-NBI, GDAs were more likely to exhibit an intralobular loop patten, whereas IDAs were more likely to exhibit a fine network pattern. In addition, the proportion of none-curative resection in GDAs was significantly higher than that in IDAs (p = 0.007). CONCLUSION: The mucin phenotype of differentiated early gastric adenocarcinoma has clinical significance. GDA was associated with less endoscopically resectability than IDA.

LncRNA STARD13-AS Expression in Gastric Cancer and its Significance.

BACKGROUND: The aim of the study is to investigate lncRNA STARD13-AS's expression and clinical characteristics in the cancer tissues of gastric cancer (GC) patients. METHODS: Microarray assessment will be used to analyze GC and non-tumor tissues. The lncRNA STARD13-AS expression in 82 GC and non-tumor tissues were measured by RT-qPCR and ISH assay. The differential expression of lncRNA STARD13-AS between the two groups and the relationship with clinical characteristics and prognosis were analyzed statistically. RESULTS: By microarray assessment, lncRNA STARD13-AS was significantly down-regulated in tumor tissues. Compared with non-tumor tissues, using both RT-qPCR and ISH assay, STARD13-AS expression was significantly depressed in GC tissues (p < 0.01, respectively) and was closely correlated with tumor stage and histological grade (p < 0.05, respectively), but was not correlated with gender, age, tumor size, tumor location or lymph node metastasis. The 5-year overall survival and progression free survival rates of the low lncRNA STARD13-AS expression group were significantly down-regulated compared with those of the high lncRNA STARD13-AS expression group (p < 0.001, respectively). CONCLUSIONS: The expression of lncRNA STARD-AS is depressed in gastric cancer tissues; the expression of lnc-RNA STARD-AS is correlated to tumor stage and degree of tumor differentiation, and may be a new molecular marker for the diagnosis, treatment, and prognosis in GC.