Summary
This systematic review synthesises Mendelian randomisation studies investigating causal relationships between modifiable risk factors and endometrial cancer incidence. The authors leverage genetic variation as an instrumental variable to overcome confounding and reverse causality limitations inherent in observational epidemiology. The evidence indicates that metabolic factors (type 2 diabetes, elevated BMI, insulin levels), hormonal markers (testosterone, cortisol), and inflammatory markers are causally associated with increased endometrial cancer risk, whilst later menarche and higher SHBG are protective.
UK applicability
Findings are applicable to UK clinical and public health practice, as endometrial cancer incidence has been rising in high-income countries including the United Kingdom. The identification of modifiable metabolic and hormonal risk factors provides potential targets for prevention strategies and clinical intervention in UK healthcare settings.
Key measures
Causal associations between risk factors (type 2 diabetes, BMI, PAI-1, fasting insulin, testosterone, cortisol, telomere length) and endometrial cancer risk; protective factors (age of menarche, TNF, LDL cholesterol, SHBG)
Outcomes reported
The review identified genetic and biochemical risk and protective factors for endometrial cancer through synthesis of Mendelian randomisation studies. Key causal associations were established between modifiable and non-modifiable exposures and endometrial cancer risk.
Topic tags
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