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Background Testicular cancer severely affects male health, so finding effective diagnosis and prognostic indicators and exploring its pathogenesis are very important. Purpose This study aims to explore the hub genes that play important roles in the occurrence and development of testicular germ cell tumor (TGCT). Methods Data were obtained from Gene Expression Omnibus datasets (GSE3218 and GSE1818) and verified in The Cancer Genome Atlas database and the Genotype-Tissue Expression database and the Human Protein Atlas database. A protein–protein interaction network was constructed to obtain hub genes. GEO2R, R software and packages were used to analyze differentially expressed genes (DEGs), receiver operating characteristic curve assessment, Cox regression analysis, Kaplan–Meier survival curve assessment, Gene Ontology analysis, Kyoto Encyclopedia of Genes and Genomes analysis, the relationship with clinicopathological information, gene set enrichment analysis, the correlation with immune cells’ infiltration, and the expression in pan-cancers of the hub genes. Results PLK4, TRIP13, TPR, KIF18A, CDKN3, HMMR, PBK, PTTG1, CKS2, SYCP1, HSPA2 , and MKI67 were selected as the hub genes. mRNA of PLK4, TRIP13, CDKN3, SYCP1, HSPA2 , and MKI67 had high diagnostic values, and higher expression of CDKN3 and HSPA2 mRNA were poor prognostic factors for progression-free interval of TGCT. The hub genes involved organelle division and cell cycle, chromosome and centromeric region, heat shock protein binding, and more. Downregulated TPR and PLK4 were selected as research targets for continued study, and they may participate in multiple signaling pathways. The expression of TPR and PLK4 correlated with the infiltration of a variety of immune cells and differed in pan-cancers. Conclusion The mRNA levels of multiple hub genes have high diagnostic and prognostic values for TGCT. TPR and PLK4 may play a role in the occurrence and development of TGCT through cancer-related signaling pathways.

Stereotactic gamma-ray body radiation therapy was found to be safe and effective in the treatment of asynchronous bRCC. Improved prognosis will require individualised treatment and a combination of multiple therapeutic approaches; this will be a primary research trend in the future.

Objective. To assess the clinical efficacy of programmed death 1 (PD-1) inhibitors plus split-course radiotherapy in the first-line treatment of advanced kidney cancer. Methods. In this prospective, randomized, single-blinded, controlled trial, 44 patients with advanced kidney cancer initially treated in our hospital from January 2017 to December 2018 were recruited. They were concurrently and randomly assigned at a ratio of 1 : 1 to the control group and the study group, with 22 cases in each group. The control group received PD-1 inhibitor nivolumab combined with ipilimumab, and the study group received split-course radiotherapy plus. The primary endpoint is clinical efficacy, and the secondary endpoints are progression-free survival (PFS), overall survival (OS), and adverse events (AEs). Results. Nivolumab plus split-course radiotherapy was associated with an objective remission rate (ORR) of 59.09% versus nivolumab alone with an ORR of 27.27%. The median PFS was 21.5 months (95% CI: 14.1—NA) after single nivolumab therapy and 28.1 months (95% CI: 24.5—NA) after nivolumab plus split-course radiotherapy, with an HR of 1.875 (95% CI: 0.877–4.011). The median OS was 27.1 months (95% CI: 20.7—NA) after single nivolumab therapy and not reached after nivolumab plus split-course radiotherapy and an HR of 2.56 (95% CI: 1.081–6.06). Nivolumab was associated with significantly better OS plus split-course radiotherapy versus nivolumab alone. Conclusion. Nivolumab plus split-course radiotherapy in patients with advanced renal cell carcinoma significantly improves ORR and prolongs overall survival with a good safety profile.

circular rna (circrna) molecules are noncoding rnas with unique circular covalently closed structures that contribute to gene expression regulation, protein translation and act as microrna sponges. circrnas also have important roles in human disease, particularly tumorigenesis and antitumor processes. Methylation is an epigenetic modification that regulates the expression and roles of dna and coding rna and their interactions, as well as of noncoding rna molecules. Previous studies have focused on the effects of methylation modification on circRNA expression, transport, stability, translation and degradation of circrnas, as well as how circrna methylation occurs and the influence of circRNAs on methylation modification processes. circRNA and methylation can also regulate disease pathogenesis via these interactions. In the present study, we define the relationship between circrnas and methylation, as well as the functions and mechanisms of their interactions during disease progression. Contents1. introduction 2. literature search strategy 3. dna methylation 4. rna methylation 5. effects of methylation on circrna biological function 6. Study of methylation-modified circRNAs in disease 7. circRNAs influence disease progression via methylation regulation 8. databases related to circrna methylation research 9. conclusion