Hyperglycemia (high blood glucose) is known to induce gene mutation and reactive oxygen species (ROS) induced DNA damage may be involved in this process of diabetes associated carcinogenesis. Recent studies on a large cohort have shown a possible link between increased cancer risk and elevated level of fasting glucose. Tumors are characterized by an increased glucose uptake and a high rate of glycolysis leading to non enzymatic glycation of proteins. Glycation is an important source of glyoxal and methylglyoxal, which leads to the formation of protein advanced glycation end products (AGEs) such as N-carboxymethyllysine (CML). CML has been detected in several human tumors using specific antibodies. The proteasome degradation of CML adducts is not complete and remnants may accumulate and cause epigenetic changes as well as further DNA and protein damage. High incidence of cancer has been reported involving AGEs in patients with chronic renal failure due to increased intracellular free radical activity. Type 2 diabetes is associated with an increased risk of cancers of the liver, pancreas, colon, kidney, breast and endometrium. Another recent study suggests that risk of pancreatic cancer is similarly elevated in people with both Type 1 and Type 2 diabetes.