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  1. Home
  3. Research Domains
  5. Biomedical And Clinical Sciences
  7. Oncology And Carcinogenesis
  9. Predictive And Prognostic Markers
  11. Appraising The Role Of Previously Reported Risk Factors In Epithelial Ovarian Cancer Risk: A Mendelian Randomization Analysis.
  1. Home
  3. Research Domains
  5. Biomedical And Clinical Sciences
  7. Oncology And Carcinogenesis
  9. Predictive And Prognostic Markers
  11. Appraising The Role Of Previously Reported Risk Factors In Epithelial Ovarian Cancer Risk: A Mendelian Randomization Analysis.

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Appraising the role of previously reported risk factors in epithelial ovarian cancer risk: A Mendelian randomization analysis.

James Yarmolinsky1,2, Caroline L Relton1,2,3, Artitaya Lophatananon4

  • 1MRC Integrative Epidemiology Unit, University of Bristol, Bristol, United Kingdom.

Plos Medicine
|August 8, 2019

View abstract on PubMed

Summary
This summary is machine-generated.

Mendelian randomization (MR) identified genetic liability to endometriosis and lifetime smoking as risk factors for invasive epithelial ovarian cancer. Different risk factors were associated with specific ovarian cancer histotypes, suggesting varied causes.

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Area of Science:

  • Genetics and Epidemiology
  • Cancer Research
  • Reproductive Health

Background:

  • Observational studies suggest various risk factors for epithelial ovarian cancer, but causal links are unclear due to confounding and reverse causation.
  • Mendelian randomization (MR) offers a method to strengthen causal inference by using genetic variants as proxies for risk factors.

Purpose of the Study:

  • To evaluate the causal association of 12 previously reported risk factors with invasive epithelial ovarian cancer risk.
  • To investigate associations with specific invasive epithelial ovarian cancer histotypes and low malignant potential tumors.

Main Methods:

  • Utilized Mendelian randomization (MR) with genetic instruments (SNPs) for 12 risk factors, including genetic liability to endometriosis, polycystic ovary syndrome, and type 2 diabetes.
  • Analyzed summary statistics from the Ovarian Cancer Association Consortium (OCAC) for invasive epithelial ovarian cancer (22,406 cases) and low malignant potential tumors (3,103 cases).
  • Employed inverse-variance-weighted models and performed sensitivity analyses (MR-Egger, weighted median/mode) with Bonferroni correction for significance.

    • Main Results:

    • Strong evidence linked genetic liability to endometriosis (OR 1.10) and suggestive evidence linked lifetime smoking (OR 1.36) to increased invasive epithelial ovarian cancer risk.
    • Significant associations were found for height with clear cell carcinoma (OR 1.36), age at menopause with endometrioid carcinoma (OR 1.09), and PCOS liability with endometrioid carcinoma (OR 0.89).
    • Limited evidence supported associations for type 2 diabetes liability, parity, or vitamin D/SHBG levels with ovarian cancer or its subtypes.

    Conclusions:

    • MR analysis supports a role for a few specific risk factors in invasive epithelial ovarian cancer, with distinct etiological drivers for different histotypes.
    • Further research is needed to identify novel risk factors crucial for the prevention of epithelial ovarian cancer.