Background

Diabetes mellitus (DM) is a group of metabolic diseases characterised by high blood sugar, either because the pancreas does not produce enough insulin or because the body does not adequately respond to the insulin that is produced. In type 1 diabetes mellitus (T1DM), autoimmune-mediated destruction of pancreatic b-cell islets leads to absolute insulin deficiency. In type 2 diabetes mellitus (T2DM), insufficient insulin is produced, the body becomes resistant to normal or even high levels of insulin, or both. In the year 2010, approximately 285 million adults had DM worldwide (6.4% of all people), and this value is predicted to rise to around 439 million (7.7%) by 2030.

Management of DM involves the control of blood glucose and lipid concentrations, blood pressure, bodyweight and smoking, as well as regular screening for complications. One of the treatment options for diabetic patients is the use of insulin and insulin analogues.  

Diabetes and cancer risk
Cancer and diabetes are diagnosed within the same individual more frequently than would be expected by chance, even after adjusting for age. Some cancers develop more commonly in patients with diabetes (predominantly type 2), whereas prostate cancer occurs less often in men with diabetes. The relative risks imparted by diabetes are greatest (approximately 2-fold or higher) for cancers of the liver, pancreas, and endometrium, and lesser (approximately 1.2-fold to 1.5- fold) for cancers of the colon/rectum, breast, and bladder. Other cancers (e.g., those of the lung) do not appear to be associated with an increased risk in diabetes, and the evidence for others (e.g., kidney and non-Hodgkin lymphoma) is inconclusive. Only few studies have explored links between T1DM and cancer.

Insulins and cancer risk
Insulin is a growth factor, and it is biologically plausible that high levels of endogenous insulin and/or exposure to administered insulin could stimulate neoplastic growth. A growth-promoting effect of insulin on cancer cells has been known for more than 30 years, with these findings pre-dating the commercial availability of insulin analogues or even of recombinant human insulin. The most plausible hypothesis concerning the mechanism underlying the potential link between insulin and related peptide hormones and cancer growth is that these act through the insulin and insulin like growth factor (IGF) 1 receptors to stimulate cell growth and inhibit apoptosis.