Suhong Li1, Ao Lin2, Dandan Han1, Haixia Zhou3, Jiwen Cheng4, Jiao Zhang5, Wen Fu2, Zhenjian Zhuo2, Jing He2. 1. Department of Pathology, Children Hospital and Women Health Center of Shanxi, Taiyuan, Shannxi, China. 2. Department of Pediatric Surgery, Guangzhou Institute of Pediatrics, Guangdong Provincial Key Laboratory of Research in Structural Birth Defect Disease, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, Guangdong, China. 3. Department of Hematology, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China. 4. Department of Pediatric Surgery, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China. 5. Department of Pediatric Surgery, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Abstract
BACKGROUND: Wilms tumor, a frequently occurring pediatric renal cancer worldwide, originated from the embryonal nephric mesenchyme. However, epidemiological data on the association between LINC00673 polymorphisms and Wilms tumor risk are scant. This case-control study was conducted to investigate the potential role of the LINC00673 rs11655237 C>T polymorphism in the susceptibility to Wilms tumor. METHODS: In the present study, we conducted a genotyping analysis of LINC00673 rs11655237 C>T in 414 cases and 1199 controls recruited from five hospitals in China. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) were estimated from multiple logistic regression models to determine the association of LINC00673 rs11655237 C>T polymorphism and Wilms tumor susceptibility. RESULTS: No significant association between the LINC00673 rs11655237 C>T polymorphism and Wilms tumor risk was observed (CT versus CC: adjusted OR = 0.90, 95% CI = 0.71-1.15; TT versus CC: adjusted OR = 0.86, 95% CI = 0.50-1.49; TT/CT versus CC: adjusted OR = 0.90, 95% CI = 0.71-1.13; and TT versus CC/CT: adjusted OR = 0.89, 95% CI = 0.52-1.53). We also failed to make any remarkable findings for this genotype in the stratification analysis. CONCLUSIONS: In summary, we failed to provide any evidence in favor of the significant susceptibility of rs11655237 C>T polymorphism in LINC00673 to Wilms tumor. These data could be useful for reinforcing our understanding of the potential contribution of LINC00673 rs11655237 C>T to Wilms tumor susceptibility.
BACKGROUND:Wilms tumor, a frequently occurring pediatric renal cancer worldwide, originated from the embryonal nephric mesenchyme. However, epidemiological data on the association between LINC00673 polymorphisms and Wilms tumor risk are scant. This case-control study was conducted to investigate the potential role of the LINC00673rs11655237 C>T polymorphism in the susceptibility to Wilms tumor. METHODS: In the present study, we conducted a genotyping analysis of LINC00673rs11655237 C>T in 414 cases and 1199 controls recruited from five hospitals in China. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) were estimated from multiple logistic regression models to determine the association of LINC00673rs11655237 C>T polymorphism and Wilms tumor susceptibility. RESULTS: No significant association between the LINC00673rs11655237 C>T polymorphism and Wilms tumor risk was observed (CT versus CC: adjusted OR = 0.90, 95% CI = 0.71-1.15; TT versus CC: adjusted OR = 0.86, 95% CI = 0.50-1.49; TT/CT versus CC: adjusted OR = 0.90, 95% CI = 0.71-1.13; and TT versus CC/CT: adjusted OR = 0.89, 95% CI = 0.52-1.53). We also failed to make any remarkable findings for this genotype in the stratification analysis. CONCLUSIONS: In summary, we failed to provide any evidence in favor of the significant susceptibility of rs11655237 C>T polymorphism in LINC00673 to Wilms tumor. These data could be useful for reinforcing our understanding of the potential contribution of LINC00673rs11655237 C>T to Wilms tumor susceptibility.