Research suggests statins could lower ovarian cancer risk

  • Yarmolinsky J & al.
  • JAMA
  • 18 Feb 2020

  • curated by Dawn O'Shea
  • UK Medical News
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A genetic study published in JAMA suggests long-term statin therapy could reduce the risk for epithelial ovarian cancer (EOC) among the general population and in BRCA1/2 mutation carriers.

The research, funded by Cancer Research UK, evaluated the association of genetically proxied inhibition of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase (HMGCR) the target of statins with EOC.

Single-nucleotide polymorphisms (SNPs) in HMGCR, Niemann-Pick C1-Like 1 (NPC1L1) and proprotein convertase subtilisin/kexin type 9 (PCSK9) associated with low-density lipoprotein (LDL) cholesterol were used as proxy for therapeutic inhibition of HMGCR, NPC1L1 and PCSK9.

Summary statistics were obtained for these SNPs from a genome-wide association study (GWAS) meta-analysis of case-control analyses of invasive EOC in the Ovarian Cancer Association Consortium (N=63,347) and from a GWAS meta-analysis of retrospective cohort analyses of EOC among BRCA1/2 mutation carriers in the Consortium of Investigators of Modifiers of BRCA1/2 (N=31,448).

In the primary analysis, genetically proxied HMGCR inhibition equivalent to a 1 mmol/L reduction in LDL cholesterol was associated with lower odds of EOC (OR, 0.60; 95% CI, 0.43-0.83; P=.002).

In BRCA1/2 mutation carriers, genetically proxied HMGCR inhibition was associated with lower ovarian cancer risk (HR, 0.69; 95% CI, 0.51-0.93; P=.01).

In secondary analyses, there were no significant associations of genetically proxied inhibition of NPC1L1 (OR, 0.97; 95% CI, 0.53-1.75; P=.91), PCSK9 (OR, 0.98; 95% CI, 0.85-1.13; P=.80) or circulating LDL cholesterol (OR, 0.98; 95% CI, 0.91-1.05; P=.55) with EOC.

However, the authors said these findings do not indicate risk reduction from medications that inhibit HMGCR. They advised that further research is needed to understand whether there is a similar association with such medications.