The role of obesity, type 2 diabetes, and metabolic factors in pancreatic cancer: A Mendelian Rando

Pancreatic cancer has a multifactorial etiology, like insulin resistance which is related to many of the risk factors including obesity, diabetes and metabolic syndrome, etc. Other factors such as tobacco, alcohol, pancreatitis and hepatitis virus infection are known triggers of inflammation, another established pathway. About two-thirds of the major risk factors are potentially modifiable, affording opportunities for preventing one of our deadliest cancer.

This study aims to evaluate the causal relationship between metabolic risk factors and pancreatic cancer within a Mendelian Randomization (MR) framework. MR is a technique for using genetic variants associated with the exposure of interest to estimate the causal relationship between exposure and outcome. If there is an association between the genetic instrument and outcome, then there is assumed to be a causal relationship between the interested exposure and outcome, because, unlike in the observational association, the genetic variant is not subject to issues of reverse causation and/or confounding.

The researchers found that increases in BMI and fasting insulin are causally associated with an increased risk of pancreatic cancer and provided little support for a causal role of type 2 diabetes or dyslipidemia in pancreatic cancer. These findings provide important evidence on the etiology of pancreatic cancer and novel pace for primary prevention to reduce the incidence and consequence of the disease.

Original article: Robert Carreras-Torres et al (2017) The Role of Obesity, Type 2 Diabetes, and Metabolic Factors in Pancreatic Cancer: A Mendelian Randomization Study, JNCI Volume 109, Issue 9, 1 September 2017, djx012