Causal effects of endometriosis on cancer risk: A Mendelian randomization study

Tianyou Tang, Huilin Yu, Yu H, Xu S, Sipei Xu, Zhong Y, Yi Zhong, Jie Ma, Ma J, Zhao T, Tingting Zhao
International journal of cancer · 2024 · vol. 154(11) , pp. 1948–1954 · doi:10.1002/ijc.34876 · PMID:38323658 · W4391604661
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This Mendelian randomization study found that genetic predisposition to endometriosis causally increases the risk for ovarian cancer while decreasing the risk for skin, hematological, and ER- breast cancers.

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Abstract

Endometriosis has been reported in epidemiological studies to be associated with certain types of cancer. However, the presence of reverse causality and residual confounding due to common risk factors introduces uncertainty regarding the extent to which endometriosis itself contributes to the development of cancer. We performed the Mendelian randomization (MR) to investigate the causal associations between endometriosis and 34 different types of cancers. The results of the inverse-variance-weighted (IVW) model suggested that genetic predisposition to endometriosis was causally associated with an increased risk for ovarian cancer (OR = 3.2913; p-value = .0320). The genetic liabilities to endometriosis had causal associations with the decreased risk for skin cancer (OR = 0.9973; p-value = .0219), hematological cancer (OR = 0.9953; p-value = .0175) and ER- breast cancer (OR = 0.6960; p-value = .0381). The causal association of the above combinations were robust by test of heterogeneity and pleiotropy. Together, our study suggests that endometriosis had causal effect on cancer risk.

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Condition tags

endometriosis

MeSH descriptors

Breast Neoplasms Breast Neoplasms Breast Neoplasms Breast Neoplasms Breast Neoplasms Breast Neoplasms Breast Neoplasms Breast Neoplasms Breast Neoplasms Breast Neoplasms Breast Neoplasms Breast Neoplasms Breast Neoplasms Breast Neoplasms Breast Neoplasms Breast Neoplasms Breast Neoplasms Breast Neoplasms Breast Neoplasms Breast Neoplasms

Citation neighborhood (2-hop)

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. Outer rings show 2-hop neighbours — papers reached through the immediate citers/citees. [ collapse to 1-hop ]

References (44)

Source provenance

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