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BACKGROUND: The purpose of the present study was to investigate the role of the 5-Fluorouracil (5-FU) resistance-related factor dihydropyrimidine dehydrogenase (DPD) in tumor immunity and prognosis and to study the relationship between drug resistance and the immune microenvironment of colon cancer. METHODS: Bioinformatics methods were used to analyze the expression of DPD associated with prognosis, immunity, microsatellite instability, and tumor mutational burden in colon cancer. Immunohistochemistry (IHC) was used to detect DPD, MLH1, MSH2, MSH6, and PMS2 in 219 colon cancer tissue samples. Additional IHC analyses were conducted to detect CD4, CD8, CD20, and CD163 in 30 colon cancer tissue samples with the most extensive immune infiltration. The significance of the correlations and clinical significance of DPD with immune infiltration, immune-related markers, microsatellite instability-related indicators, and prognosis were evaluated. RESULTS: The major findings of the present study are as follows: (1) DPD was expressed in tumor and immune cells and associated with certain immune cell-related markers, particularly M2 macrophages that expressed CD163. (2) DPD expression significantly and positively correlated with immune cell markers and immune checkpoints PD-1 and PD-L1. High expression of DPD in immune cells, but not tumor cells, led to increased immune infiltration. (3) High expression of DPD in immune and tumor cells induced 5-FU resistance and was associated with unfavorable prognosis. (4) DPD expression closely correlated with microsatellite instability and tumor mutational burden and led to resistance to 5-FU in patients with microsatellite instability. (5) Bioinformatics analyses revealed that DPD was enriched in immune-related functions and pathways such as activation of T cells and macrophages. CONCLUSIONS: DPD plays an important role in the immune microenvironment and drug resistance of colon cancers and their functional association.

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BACKGROUND: Much research has focused on detecting microsatellite instability (MSI), which is frequently employed in the diagnosis and treatment of patients with colon cancer. However, the causes and progression of MSI in colon cancer have not yet been thoroughly elucidated. In this study, we screened and validated the genes associated with MSI in colorectal adenocarcinoma (COAD) using bioinformatics analysis. METHODS: MSI-related genes of COAD were obtained from the Gene Expression Omnibus dataset, Search Tool for the Retrieval of Interaction Gene/Proteins, Gene Set Enrichment Analysis, and Human Protein Atlas. The function, prognostic value, and immune connection of MSI-related genes in COAD were examined using Cytoscape 3.9.1, the Human Gene Database, and the Tumor IMmune Estimation Resource. Key genes were verified using The Cancer Genome Atlas database and immunohistochemistry of clinical tumor samples. RESULTS: We identified 59 MSI-related genes in patients with colon cancer. The protein interaction network of these genes was developed, and numerous functional modules associated with MSI were discovered. Pathways related to MSI were identified using KEGG enrichment analysis, and these included chemokine signaling, thyroid hormone synthesis, cytokine receptor interaction, estrogen signaling, and Wnt signaling pathways. Further analyses were used to identify the MSI-related gene, glutathione peroxidase 2 (GPX2), which was closely related to the occurrence of COAD and tumor immunity. CONCLUSIONS: In COAD, GPX2 may be crucial for the establishment of MSI and tumor immunity, and its deficiency may result in MSI and immune cell infiltration in colon cancer.

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BACKGROUND: Leiomyoma of the seminal vesicle is a rare leiomyoma characterized by the formation of benign leiomyomatous tissue within the seminal vesicle. Although histologically benign, excessive size can lead to urinary system disease if left untreated. Herein, we report a case of a seminal vesicle epithelioid leiomyoma. CASE PRESENTATION: A 36-year-old Chinese man sought medical attention at our hospital for urination pain and hemospermia. CT showed a 5.3 cm × 5.0 cm seminal vesicle mass with a mixed density in the right seminal vesicle. The gross specimen showed light yellow, gray, and white tissues, with softness and hemorrhage in some places. Histologically, it showed classic spindle cell proliferation, with spindle cells arranged in fascicles, and mitosis was rare. Immunohistochemistry showed frequent expression of smooth muscle markers, such as calponin, SMA, and desmin. A diagnosis of epithelioid leiomyoma was proposed according to the immunohistochemical findings and morphology. The patient did not receive adjuvant therapy. There was no evidence of tumor recurrence in the 10 months after surgery. CONCLUSIONS: We report the first case of epithelioid leiomyoma in the seminal vesicle. This disease should be included in the differential diagnostic list of seminal vesicle tumors with epithelioid morphology.

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BACKGROUND: Colon adenocarcinoma (COAD) is one of the most common malignancies. To identify candidate genes that may be involved in colon adenocarcinoma development and progression, weighted gene co-expression network analysis (WGCNA) was used to construct gene co-expression networks to explore associations between gene sets and clinical features and to identify candidate biomarkers. Moreover, we intend to make a preliminary exploration on it. METHODS: Gene expression profiles and clinical information were collected from The Cancer Genome Atlas COAD database for analysis. The gene expression profiles of GSE106582 and GSE110224 were screened from the Gene Expression Omnibus database for verification. WGCNA analysis, functional pathway enrichment analysis, and prognosis analysis were performed on three databases. Target genes were selected from the key genes for experimental verification and research. RESULTS: Key genes obtained by WGCNA analysis were mainly enriched in key functions and pathways such as drug metabolism, steroid hormones, and retinol metabolism. A total of four prognostic genes were screened out: SELENBP1, NAT2, VSIG2, and CES2. VSIG2 was selected as the target gene for experimental verification, and its encoded protein was found to be mainly expressed in immune cells. Its expression was positively correlated with immune infiltration. CONCLUSIONS: VSIG2 was shown to be associated with immune invasion and antigen presentation in COAD, suggesting it plays an important role in COAD development and progression. It could be used as a potential biomarker or therapeutic target for COAD.