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Background: The close relationship between colorectal cancer and inflammation has been widely reported. However, the relationship between colorectal cancer and inflammation at the genetic level is not fully understood. Method: From a genetic perspective, this study explored the relationship between inflammation-related genes and the immune microenvironment in colorectal cancer. We identified prognostic genes, namely CX3CL1 , CCL22 , SERPINE1 , LTB4R , XCL1 , GAL, TIMP1 , ADIPOQ , and CRH , by using univariate and multivariate regression analyses. A risk scoring model for inflammatory response was established, and patients in The Cancer Genome Atlas (TCGA) database and Gene Expression Omnibus (GEO) database were divided into two groups: high risk group and low risk group. Results: The analysis showed that the prognosis of the two groups was significantly different, and the low-risk group had a higher survival rate and longer survival time. Pathways related to apoptosis, inflammatory response, and hypoxia were significantly enriched as shown via Gene Set Enrichment Analysis (GSEA). Activated dendritic cell infiltration was found in both the TCGA and GEO databases, and the CCL21 gene played a significant role in the process of activated dendritic cell infiltration. CCL21 gene was also positively correlated with inflammatory response, and the gene expression and risk score were significantly different between the two groups. Conclusion: In summary, inflammatory response has a direct impact on patients with colorectal cancer in the prognosis and immune infiltration and further research studies on the inflammatory response can help in advancing the development of immunotherapy for colorectal cancer. [ABSTRACT FROM AUTHOR]

Background: Chronic inflammation and immune cell dysfunction in the tumor microenvironment are key factors in the development and progression of gastric tumors. However, inflammation-related genes associated with gastric cancer prognosis and their relationship with the expression of immune genes are not fully understood. Method: In this study, we established an inflammatory response model score called "Riskscore", based on differentially expressed genes in gastric cancer. We used Survival and Survminer packages in R to analyze patient survival and prognosis in risk groups. The survival curve was plotted using the Kaplan–Meier method, and the log-rank test was used to assess statistical significance, and we performed the ROC analysis using the R language package to analyze the 1-, 3-, and 5-year survival of patients in the GEO and TCGA databases. Single-factor and multi-factor prognostic analyses were carried out for age, sex, T, N, M, and risk score. Pathway enrichment analysis indicated immune factor-related pathway enrichment in both patient groups. Next, we screened for important genes that are involved in immune cell regulation. Finally, we created a correlation curve to explore the correlation between Riskscore and the expression of these genes. Results: The prognosis was significantly different between high- and low-risk groups, and the survival rate and survival time of the high-risk group were lower than those of the low-risk group. we found that the pathways related to apoptosis, hypoxia, and immunity were most enriched in the risk groups. we found two common tumor-infiltrating immune cell types (i.e., follicular helper T cells and resting dendritic cells) between the two risk groups and identified 10 genes that regulate these cells. Additionally, we found that these 10 genes are positively associated with the two risk groups. Conclusion: Finally, a risk model of the inflammatory response in gastric cancer was established, and the inflammation-related genes used to construct the model were found to be directly related to immune infiltration. This model can improve the gastric cancer prognosis prediction. Our findings contribute to the development of immunotherapy for the treatment of gastric cancer patients. [ABSTRACT FROM AUTHOR]

Background: Imbalanced nutritional supply and demand in the tumor microenvironment often leads to hypoxia. The subtle interaction between hypoxia and immune cell behavior plays an important role in tumor occurrence and development. However, the functional relationship between hypoxia and the tumor microenvironment remains unclear. Therefore, we aimed to investigate the effect of hypoxia on the intestinal tumor microenvironment. Method: We extracted the names of hypoxia-related genes from the Gene Set Enrichment Analysis (GSEA) database and screened them for those associated with colorectal cancer prognosis, with the final list including ALDOB , GPC1 , ALDOC , and SLC2A3. Using the sum of the expression levels of these four genes, provided by The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases, and the expression coefficients, we developed a hypoxia risk score model. Using the median risk score value, we divided the patients in the two databases into high- and low-risk groups. GSEA was used to compare the enrichment differences between the two groups. We used the CIBERSORT computational method to analyze immune cell infiltration. Finally, the correlation between these five genes and hypoxia was analyzed. Result: The prognosis of the two groups differed significantly, with a higher survival rate in the low-risk group than in the high-risk group. We found that the different risk groups were enriched by immune-related and inflammatory pathways. We identified activated M0 macrophages in TCGA and GEO databases and found that CCL2/4/5 , and CSF1 contributed toward the increased infiltration rate of this immune cell type. Finally, we observed a positive correlation between the five candidate genes' expression and the risk of hypoxia, with significant differences in the level of expression of each of these genes between patient risk groups. Conclusion: Overall, our data suggest that hypoxia is associated with the prognosis and rate of immune cell infiltration in patients with colorectal cancer. This finding may improve immunotherapy for colorectal cancer. [ABSTRACT FROM AUTHOR]