IGFs, diabetes and cancer

This page has now been adopted by Jeff Holly and is under construction.

It has long been known that some cancers, breast, prostate and endometrium included, are responsive to hormonal signals. More recently it has been recognised that potentially carcinogenic mutations are relatively common in the elderly population, whereas progression to clinical cancer is relatively uncommon. This progression is largely influenced by the nutritional, metabolic and endocrine milieu, which mediates many of the environmental influences upon cancer progression. Tumour cells entering the growth pathway have acquired gene mutations which enable them to co-opt physiological cell signalling systems and use them to their own advantage. This may involve aberrant expression of receptors, aberrant responses to their stimulation, or aberrant hormone production. Many hormones and other cell signalling systems affect tumour regulation. Prominent among these is the insulin-IGF axis, which mediates both growth and metabolism. Insulin secretion from the pancreas suppresses hepatic production of sex hormone binding globulin (SHBG) and IGF binding protein-1 (IGF-BP1), resulting in increased availability of sex steroids and IGF-1. Diabetes-related cancers in general over-express and aberrantly express the insulin and IGF receptors and are responsive to their signals. This article reviews the contribution of the IGF signalling pathway to cancer development in diabetes.