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Background: Five-year ovarian cancer survival rates are below 50%; there is considerable interest in whether common medications like statins may improve survival.Methods: We identified women diagnosed with ovarian cancer in Australia from 2003 to 2013 through the Australian Cancer Database and linked these records to national medication and death databases. We used Cox proportional hazards regression to estimate hazard ratios (HR) and confidence intervals (CI) for associations between statins and survival.Results: Pre-diagnosis statin use was not associated with survival overall but was associated with better survival among women with endometrioid cancers. Statin use after diagnosis was associated with better ovarian cancer-specific survival (OVS, HR = 0.87, 95%CI 0.81-0.94), but this association was largely restricted to women who started using statins after their cancer diagnosis (OVS HR = 0.68, 0.57-0.81 vs. HR = 0.94, 0.87-1.01 for continuing users). The association was strongest for endometrioid cancers (OVS HR = 0.48, 0.29-0.77).Conclusions: Use of statins may confer a survival benefit for women with ovarian cancer but it is impossible to rule out bias in observational studies. Particularly problematic are reverse causation where disease status affects statin use, confounding by indication and the absence of data for women with normal cholesterol levels. A randomised trial is required to provide definitive evidence. [ABSTRACT FROM AUTHOR]

Previous Mendelian randomization (MR) studies on 25-hydroxyvitamin D (25(OH)D) and cancer have typically adopted a handful of variants and found no relationship between 25(OH)D and cancer; however, issues of horizontal pleiotropy cannot be reliably addressed. Using a larger set of variants associated with 25(OH)D (74 SNPs, up from 6 previously), we perform a unified MR analysis to re-evaluate the relationship between 25(OH)D and ten cancers. Our findings are broadly consistent with previous MR studies indicating no relationship, apart from ovarian cancers (OR 0.89; 95% C.I: 0.82 to 0.96 per 1 SD change in 25(OH)D concentration) and basal cell carcinoma (OR 1.16; 95% C.I.: 1.04 to 1.28). However, after adjustment for pigmentation related variables in a multivariable MR framework, the BCC findings were attenuated. Here we report that lower 25(OH)D is unlikely to be a causal risk factor for most cancers, with our study providing more precise confidence intervals than previously possible. Studies of the genetic association between vitamin D and cancer risk have typically been underpowered. Here the authors analyse this using Mendelian Randomisation with more than 70 vitamin D variants obtained from the UK Biobank and large-scale data from various consortia, confirming null associations between vitamin D and most cancers. [ABSTRACT FROM AUTHOR]

Background: Observational studies suggest greater height is associated with increased ovarian cancer risk, but cannot exclude bias and/or confounding as explanations for this. Mendelian randomisation (MR) can provide evidence which may be less prone to bias.Methods: We pooled data from 39 Ovarian Cancer Association Consortium studies (16,395 cases; 23,003 controls). We applied two-stage predictor-substitution MR, using a weighted genetic risk score combining 609 single-nucleotide polymorphisms. Study-specific odds ratios (OR) and 95% confidence intervals (CI) for the association between genetically predicted height and risk were pooled using random-effects meta-analysis.Results: Greater genetically predicted height was associated with increased ovarian cancer risk overall (pooled-OR (pOR) = 1.06; 95% CI: 1.01-1.11 per 5 cm increase in height), and separately for invasive (pOR = 1.06; 95% CI: 1.01-1.11) and borderline (pOR = 1.15; 95% CI: 1.02-1.29) tumours.Conclusions: Women with a genetic propensity to being taller have increased risk of ovarian cancer. This suggests genes influencing height are involved in pathways promoting ovarian carcinogenesis. [ABSTRACT FROM AUTHOR]