J Cancer 2019; 10(20):4860-4865. doi:10.7150/jca.32675
Genetic variations in MAGE-A11 predict the risk and survival of renal cell cancer
1. Department of Urology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China
2. Department of Biostatistics, School of Public Health, Nanjing Medical University, Nanjing, 211166, Jiangsu, China.
3. Department of Environmental Health, Harvard T.H. Chan School of Public Health, Harvard University, Boston, MA, USA.
#These authors contributed equally to this work.
Melanoma antigen-A11 (MAGE-A11) is a low-abundance, primate-specific steroid receptor coregulator in normal tissues of the human reproductive tract, which plays an important role in tumorigenesis. Single-nucleotide polymorphisms (SNPs) have been shown to contribute to cancer risk and prognosis. However, the role of SNPs of MAGE-A11 in renal cell carcinoma (RCC) has not been established. Two intronic SNPs (rs6641352 and rs6540341) of MAGE-A11 have been screened to assess their associations with RCC risk and prognosis in a case control study. We found that rs6641352 was associated with RCC susceptibility in the dominant model (TC/CC vs. TT, adjusted odds ratio = 1.315, 95% confidence interval [CI] = 1.089-1.588) and with survival of RCC in the recessive model (CC vs. TT/TC, adjusted hazard ratio = 3.526, 95% CI = 1.072-11.595). For the SNP rs6540341, individuals with the T allele could have a critically increased risk of RCC (adjusted odds ratio = 1.301, 95% CI = 1.081-1.564, P = 0.005 in the dominant model). However, there was no significant association between rs6540341 and RCC survival. Hence, rs6641352 in MAGE-A11 may contribute to the genetic susceptibility and prognosis for RCC and act as a biomarker for RCC occurrence and prognosis.
Keywords: renal carcinoma, MAGE-A11, single-nucleotide polymorphism, survival
Su S, Gu Q, Xu A, Shen S, Liu S, Zhang C, Miao C, Qin C, Liu B, Wang Z. Genetic variations in MAGE-A11 predict the risk and survival of renal cell cancer. J Cancer 2019; 10(20):4860-4865. doi:10.7150/jca.32675. Available from http://www.jcancer.org/v10p4860.htm