Moreover, a meta-analysis showed that patients with one of single nuclear polymorphisms vitamin D receptor (VDR), the FokI rs2228570 TT genotype, had a significantly higher risk for developing ovarian cancer as well as prostate, breast, skin, non-Hodgkin lymphoma, and colorectal cancer compared with its CC genotype [19, 20]. By seeking susceptibility genes and establishing high-risk populations, early diagnosis may be beneficial to improve ovarian cancer survival. EVP4593 molecular weight As tumor candidate genes, p63 and p73 are involved in the regulation of the cell cycle, apoptosis, differentiation and other critical

cellular processes. The abnormal expression of the two genes can play catalytic roles in the development of ovarian tumors and achieve synergy in terms of early malignant transformation and enhanced tumor invasion. In recent years, there has been an increased interest in research into the connection between p63 and p73 variants generated

by genetic polymorphisms and cancer progression. Meanwhile, several genetic polymorphisms have been implicated Ruboxistaurin price in the pathogenesis of ovarian cancer [14–20]. However, little is known about how the p63 and p73 polymorphisms are involved in ovarian cancer susceptibility and clinical pathology. Therefore, we conducted this study to genotype three SNPs in the p63 and p73 genes to determine whether this polymorphism functioned as a modifier of ovarian cancer development. Prior studies have demonstrated that p63 and p73 were highly expressed in female germ cells during meiotic arrest and play an important role in DNA damage-induced apoptosis in female germ cells

[21, 22]. Recently, three SNPs (rs873330 T > C, rs4648551 G > A, rs6695978 G > A) located in p63 and p73 were identified, and they appear to be under evolutionary selection pressures using the criteria of Atwal [23, 24] and information theory. That study showed a clear enrichment of the SNPs in infertility and IVF patients and revealed that polymorphisms in the human p63 and p73 genes could be involved in reproductive deficits [11, 25]. In theory, the factors including non-pregnancy, infertility and application of ovulation induction drugs that Silibinin lead to continued ovulation can increase the incidence of ovarian cancer [26]. Infertility therapies utilize products, such as IVF, that alter the hormonal balance and may also increase the risk of ovarian tumors [12]. Based on the close relationship between infertility and ovarian cancer susceptibility, we genotyped these SNPs in ovarian cancer patients and normal individuals using a case–control study. Our results indicated that the A allele frequency in p73 rs6695978 G > A was statistically higher in the case group compared with the control group.