Abstract
We aimed to analyze the association between excision repair cross-complementing rodent repair deficiency complementation group 1 (XRCC1) and ovarian cancer risk. We performed a hospital-based case-control study with 155 cases and 313 controls in China. All Chinese cases with newly diagnosed primary ovarian cancer between May 2005 to May 2010 in our hospital were invited to participate within 2 months of diagnosis. Controls were randomly selected from people who requested general health examinations in the same hospital during the same period. SNPs in EXCC1, ERCC1 C8092A and ERCC1 T19007C, were analyzed by PCR-RFLP method. We observed a non-significantly increased risk of ovarian cancer among individuals with ERCC1 8092TT compared with those with the 8092CC genotype (adjusted OR=1.55, 95% CI%=0.74-2.97). Moreover, 19007TT genotype carriers also showed a non-significant increased risk of ovarian cancer over those with the 19007CC genotype (adjusted OR=1.78, 95% CI%=0.91-3.64). Our firstly investigation of links between polymorphisms in the ERCC1 gene and the risk of ovarian cancer in Chinese population demonstrated no significant association. Further large sample studies in Chinese populations are needed.
Highlights
Ovarian cancer has the highest mortality rate of all female cancers; more than 50% of the 21,650 women diagnosed with ovarian cancer die annually from this disease (Ries et al, 2007)
The distributions of the genotype frequencies were in agreement with those expected from the HardyWeinberg Equilibrium (HWE) model at the 0.05 level for controls (p=0.11 for ERCC1 C8092A and p=0.14 for ERCC1 T19007C)
We studies on the modification of the other polymorphisms did not found an significant association between the two and environment factors in the ERCC1 and other DNA
Summary
Ovarian cancer has the highest mortality rate of all female cancers; more than 50% of the 21,650 women diagnosed with ovarian cancer die annually from this disease (Ries et al, 2007). Most of the known risk factors are related to parity and family history of ovarian cancer. The DNA damage, included oxidative DNA damage, single- and double-strand breaks in DNA chains, and DNA–DNA or DNA–protein cross-links. Such damages, if not repaired, may cause errors during DNA synthesis leading tomutations that increase cancer risk (Liu et al, 2009; Rajaraman et al, 2010). Polymorphisms of DNA repair genes are plausible candidates that can modify the risk of human cancers. Previous epidemiology and experimental studies have reported that a number of single nucleotide polymorphisms (SNPs) in DNA repair genes may modify ovarian cancer (Li et al, 2001; Reed et al, 2003; Avraam et al, 2011)
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