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The association of invasive ovarian carcinoma risk with the functional polymorphism rs2228570 ( aka rs10735810; FokI polymorphism) in the vitamin D receptor ( VDR) gene was examined in 1820 white non-Hispanic cases and 3479 controls in a pooled analysis of five population-based case-control studies within the Ovarian Cancer Association Consortium. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using unconditional logistic regression. Carriers of the rare T allele were at increased risk of ovarian carcinoma compared to women with the CC genotype in all studies combined; each copy of the T allele was associated with a modest 9% increased risk (OR = 1.09; 95% CI: 1.01-1.19; p = 0.04). No significant heterogeneity among studies was observed ( p = 0.37) and, after excluding the dataset from the Hawaii study, the risk association for rs2228570 among replication studies was unchanged (OR = 1.09; 95% CI: 1.00-1.19; p = 0.06). A stronger association of rs2228570 with risk was observed among younger women (aged < 50 years versus 50 years or older) ( p = 0.04). In all studies combined, the increased risk per copy of the T allele among younger women was 24% (OR = 1.24; 95% CI: 1.04-1.47; p = 0.02). This association remained statistically significant after excluding the Hawaii data (OR = 1.20; 95% CI: 1.01-1.43; p = 0.04). No heterogeneity of the association was observed by stage ( p = 0.46), tumor histology ( p = 0.98), or time between diagnosis and interview ( p = 0.94). This pooled analysis provides further evidence that the VDR rs2228570 polymorphism might influence ovarian cancer susceptibility. [ABSTRACT FROM AUTHOR]

The article offers information on a study regarding the incidence of hereditary non-polyposis colorectal cancer syndrome (HNPCC)-related gene mutations in patients with familial ovarian cancer. The study was conducted on patients who had previously tested negative for breast cancer gene mutations. It has been concluded that HNPCC should be taken into consideration during the evaluation of patients with suspected ovarian cancer and whose breast cancer mutation testing had been negative.

Aim: The role of human papillomavirus (HPV) infection in ovarian tumorigenesis is uncertain. The objective of this study was to screen a collection of ovarian tumors for the presence of high-risk oncogenic HPV types 16, 18 and 33. Methods: Twenty benign and malignant ovarian tumors were obtained from women undergoing pelvic surgery at a regional comprehensive cancer institution in North America. DNA was isolated from the snap-frozen tumors, and commercial polymerase chain reaction (PCR) detection sets were used to analyze the tumor DNA samples for the presence of DNA from HPV types 16, 18 and 33. Results: The DNA from HPV types 16, 18 and 33 was not detected in any of the ovarian tumors. Conclusions: Our findings do not support an association between infection with HPV types 16, 18 and 33 and ovarian neoplasia in this patient population. [ABSTRACT FROM AUTHOR]

Both 9-β-D-arabinofuranosyladenine 5′-triphosphate (aATP) and 1-β-D-arabinofuranosylcytosine 5′-triphosphate (aCTP) inhibit terminal deoxynucleotidyl transferase and DNA polymerases α and β but not DNA polymerase γ from human cells. Inhibition of terminal deoxynucleotidyl transferase by both compounds is competitive with respect to either dGTP, dCTP, dATP, or dTTP and inhibition of DNA polymerases α and β is competitive with respect to dATP (for aATP) and dCTP (for aCTP). The inhibition constants for aATP for each enzyme are lower than the inhibition constants for aCTP implying that aATP has a stronger affinity for each enzyme than aCTP. In addition, the inhibition constants for aATP for each enzyme are about equal, suggesting that the drug binds to each enzyme with about the same affinity. The same is true for aCTP. Both compounds are non-competitive inhibitors of terminal deoxynucleotidyl transferase with respect to initiator [(dA)12-18], uncompetitive inhibitors of DNA polymerases α and β with respect to template/primer (activated DNA), and non-competitive inhibitors of DNA polymerases α and β with respect to a non-analogous substrate (dTTP). Inhibition of all three enzymes was reversed by simple dilution but not by additional enzyme, template/primer, initiator, or divalent cation. These results suggest that aATP and aCTP inhibit terminal deoxynucleotidyl transferase by competing with any substrate (dGTP, dCTP, dATP, or dTTP) for binding to the enzyme and DNA polymerases α and β by specifically competing with their analogs (dATP or dCTP) for binding to these enzymes. [ABSTRACT FROM AUTHOR]