To compare clinical characteristics and survival outcomes of patients with multiple renal cell carcinoma versus single renal cell carcinoma. Develop a prognostic model for predicting prognosis in patients with multiple tumors and analyze prognostic factors. Patients with primary multiple renal cell carcinoma were selected from the Surveillance, Epidemiology, and End Results database (2004–2015). They were divided into single-tumor and multiple-tumor groups. Survival analysis was conducted using the Kaplan–Meier method and log-rank test. A Cox regression model was used to identify potential prognostic factors. A total of 19,489 renal cell carcinoma cases were included, with 947 in the multiple-tumor group and 18,542 in the single-tumor group. The multiple-tumor group had lower cancer-specific survival (P = 0.03, HR = 1.431). Cox regression identified risk factors for the multiple-tumor group including number of tumors, gender, combined summary stage, T stage, N stage, tumor size, and type of surgery. The predicted probabilities showed acceptable agreement with the actual observations at 3-, 5-, and 8-years area under the curve values in both the training and validation cohorts (0.831 vs. 0.605; 0.775 vs. 0.672; and 0.797 vs. 0.699, respectively). Compared with single renal cell carcinoma, multiple renal cell carcinoma is associated with decreased cancer-specific survival. Additionally, we identified several prognostic factors including the number of tumors, T stage, tumor size, and type of surgery. These findings offer valuable insights for selecting appropriate treatment strategies for patients diagnosed with multiple renal cell carcinomas.

Renal cell carcinoma (RCC) is a hypermetabolic disease. Abnormal up-regulation of glycolytic signaling promotes tumor growth, and glycolytic metabolism is closely related to immunotherapy of renal cancer. The aim of the present study was to determine whether and how the glycolysis-related biomarker TCIRG1 affects aerobic glycolysis, the tumor microenvironment (TME) and malignant progression of clear cell renal cell carcinoma (ccRCC). Based on The Cancer Genome Atlas (TCGA, n = 533) and the glycolysis-related gene set from MSigDB, we identified the glycolysis-related gene TCIRG1 by bioinformatics analysis, analyzed its immunological properties in ccRCC and observed how it affected the biological function and glycolytic metabolism using online databases such as TIMER 2.0, UALCAN, LinkedOmics and in vitro experiments. It was found that the expression of TCIRG1, was significantly increased in ccRCC tissue, and that high TCIRG1 expression was associated with poor overall survival (OS) and short progression-free interval (PFI). In addition, TCIRG1 expression was highly correlated with the infiltration immune cells, especially CD4+T cell Th1, CD8+T cell, NK cell, and M1 macrophage, and positively correlated with PDCD1, CTLA4 and other immunoinhibitors, CCL5, CXCR3 and other chemokines and chemokine receptors. More importantly, TCIRG1 may regulate aerobic glycolysis in ccRCC via the AKT/mTOR signaling pathway, thereby affecting the malignant progression of ccRCC cell lines. Our results demonstrate that the glycolysis-related biomarker TCIRG1 is a tumor-promoting factor by affecting aerobic glycolysis and tumor immune microenvironment in ccRCC, and this finding may provide a new idea for the treatment of ccRCC by combination of metabolic intervention and immunotherapy.

Clear cell renal cell carcinoma (ccRCC) is a frequent malignant tumor of the kidney which has a dismal prognosis. At present, targeted therapies and immunotherapy have achieved significant results; however, the overall survival rate of patients with ccRCC remains unacceptably poor. It is therefore necessary to find novel therapeutic and diagnostic targets for ccRCC. It has been reported that enolase 2 (ENO2) is an oncogene, although its function in the immune microenvironment and in the growth of ccRCC has yet to be fully elucidated. The present study analyzed the data of patients with ccRCC both from the Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) databases, and from clinical samples obtained from Third Affiliated Hospital of the Second Military Medical University to investigate the role of ENO2 in the progression of ccRCC and the correlation between ENO2 and certain clinical features. It was found that the expression of ENO2 was elevated both in patients with ccRCC retrieved from the GEO and TCGA databases and in clinical ccRCC samples obtained from Third Affiliated Hospital of the Second Military Medical University. In addition, the prognosis of patients was poorer when ENO2 was highly expressed. Gene Ontology (GO) analysis and Gene Set Enrichment Analysis (GSEA) confirmed that ENO2 participated in the regulation of various pathways in ccRCC. In vitro experiments including Cell Counting Kit-8 cell proliferation assay, Transwell and Matrigel assays confirmed that ENO2 could promote the proliferation and migration of ccRCC cells. Furthermore, a number of immunosuppressive indicators were identified that positively correlated with ENO2 expression. In conclusion, the present study revealed that ENO2 expression promotes the proliferation, invasion and migration of ccRCC cells, and may serve as a novel predictor to evaluate prognosis and the efficacy of immune checkpoint blockade treatment for patients with ccRCC.

ObjectiveTo investigate the expressions of HSF1 and tetra-hydroxynonene (4-HNE) in prostate cancer (PCa) tissue and their clinical significance.METHODSUsing the immunohistochemical method, we detected the expressions of HSF1 and 4-HNE in the prostatic tissues of 50 cases of PCa and another 50 cases of BPH, and analyzed the relationship of the two expressions with Gleason grade.RESULTSThe positive expression level of HSF1 was dramatically higher in the highly, moderately and lowly differentiated PCa than in the BPH tissue (37.5%, 50.0% and 75.0% vs 4.0%, P = 0.001) and showed statistically significant difference among different Gleason grades (P = 0.025), so was that of 4-HNE (81.3%, 92.9% and 100.0% % vs 6.0%, P = 0.001), also with statistically significant difference among different Gleason grades (P = 0.029). There was a positive correlation between the expression of HSF1 and that of 4-HNE in the PCa tissue (r = 0.947, P = 0.001).CONCLUSIONSThe overexpressions of HSF1 and 4-HNE are related to the Gleason grades of prostate cancer, which can be used as an new biological marker with important reference value for assessing the malignancy of prostate cancer.

OBJECTIVE:To investigate the expressions of glutathione S-transferase (GSTP1) and tetra-hydroxynonenal (4-HNE) in prostate cancer (PCa) and their clinical significance.METHODS:We determined the expressions of GSTP1 and 4-HNE in 40 patients with PCa and another 42 with benign prostatic hyperplasia (BPH) by immunohistochemistry and analyzed their relationship with Gleason grades.RESULTS:The expression rate of GSTP1 was 92.9% in the BPH tissue, and those in the highly, moderately, and lowly differentiated PCa tissues were 58.3%, 20.0%, and 16.7%, respectively, significantly higher in the BPH than in the PCa group (P <0.01). However, the positive rate of 4-HNE was only 5.0% in the BPH tissue, markedly lower than 91.6%, 100.0%, and 100.0% in the highly, moderately, and lowly differentiated PCa tissues (P <0.01). There was a negative correlation between the expression of GSTP1 and that of 4-HNE in the PCa tissue (r = －2.73, P <0.01).CONCLUSIONS:Expression deletion of GSTP1 and high expression of 4-HNE may play an important role in the progression of prostate cancer.