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Qianfeng Zhuang,* Zhen Chen,* Jie Shen,* Min Fan, Dong Xue, Hao Lu, Renfang Xu, Xiaozhou He Department of Urology, The Third Affiliated Hospital of Soochow University, Changzhou 213003, China *These authors contributed equally to this work Background: This meta-analysis evaluated the clinicopathologic and prognostic significance of RASSF1A promoter methylation in renal cell carcinoma (RCC).Materials and methods: The ORs or HRs and their 95% CIs were calculated. Trial sequential analysis was conducted.Results: Twenty-two articles that included 1,421 patients with RCC and 724 controls were identified. RASSF1A promoter methylation correlated with RCC in tissue, blood, and urine samples. On multivariate analysis, RASSF1A promoter methylation was associated with tumor grade (grade 3–4 vs 1–2: OR=3.59), clinical stage (stage 3–4 vs 1–2: OR=2.15), T classification (pT2–4 vs pT1: OR=2.66), histologic subtypes (papillary vs clear cell: OR=2.91), and cancer-specific survival (HR=1.78), but it was not linked to age, gender, lymph node status, distant metastasis, or overall survival. The Cancer Genome Atlas data also showed that RASSF1A methylation was significantly more likely to be seen in papillary vs clear-cell RCC (OR=23.19).Conclusion: RASSF1A promoter methylation may be associated with the development and progression of RCC, as well as poor cancer-specific survival. Methylation was more frequent in papillary vs clear-cell RCC. More studies are needed to confirm these findings in blood or urine samples. Keywords: RAS association domain family protein 1A, methylation, survival, clinical features&nbsp

Xu Han,1,* Lianhua Piao,2,* Qianfeng Zhuang,1 Xiaofeng Yuan,3 Zhiwei Liu,3 Xiaozhou He1 1Department of Urology, The Third Affiliated Hospital of Soochow University, 2Institute of Bioinformatics and Medical Engineering, Jiangsu University of Technology, 3Department of Orthopaedics, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu, People’s Republic of China *These authors contributed equally to this work Abstract: The growing number of findings demonstrate that nuclear receptor suppressor of variegation, enhancer of zeste, and trithorax domain-containing 3 (NSD3) is amplified and overexpressed in multiple cancer types. Nevertheless, the biological roles of NSD3 in carcinogenesis have not been well understood. In this review, we summarize the current knowledge on the mechanisms underlying NSD3 regulation in different cancers. In addition, NSD3 may serve as a potential druggable target for selective cancer therapy in the future. Keywords: NSD3, cancer, carcinogenesis