The opportunity to draw upon genetic data from large-scale, international consortia allows for triangulation of evidence using distinct methodological approaches that make orthogonal underlying assumptions and suffer from distinct sources of bias. The findings of our study
support a potential causal effect of genetically predicted T2DM and/or fasting insulin levels, rather than genetically predicted fasting glucose levels, on risk of breast, endometrial, pancreatic and kidney cancer. These findings are consistent with experimental and molecular epidemiological data which support a role for insulin signalling in the development of several cancers and may therefore represent an important pathway linking T2DM and cancer.
