The inactivation of p16INK4A and
p14ARF via promoter methylation has been investigated in various
cancers. However, the clinical effects of p16INK4A and
p14ARF promoter methylation on
renal cell carcinoma (RCC) remain to be clarified. The pooled data were calculated and summarized. Finally, an investigation of 14 eligible studies with 1231 RCC patients and 689 control patients was performed. Methylated p16INK4A and
p14ARF were observed to be significantly higher in RCC than in control subjects without
malignancies (OR = 2.77, P = 0.005; OR = 11.73, P < 0.001, respectively). Methylated p16INK4A was significantly associated with the risk of RCC in the tissue subgroup, but not in the serum and urine subgroups. Methylated p16INK4A was significantly associated with
tumor size. We did not find that p16INK4A promoter methylation was associated with sex,
tumor grade, lymph node status, and
tumor histology. Methylated
p14ARF was significantly correlated with sex and
tumor histology. Three studies reported that p16INK4A methylation was not significantly correlated with the prognosis of RCC. The results suggested that p16INK4A and
p14ARF promoter methylation may be correlated with the
carcinogenesis of RCC, and that methylated
p14ARF , especially, can be a major susceptibility gene. We also found the different clinicopathological significance of 16INK4A and
p14ARF in RCC. Additional studies with sufficient data are essential to further evaluate the clinical features and prognostic effect of p16INK4A and
p14ARF promoter methylation in RCC.