TY - JOUR
T1 - The relation of type 2 diabetes and cancer
AU - Strickler, H. D.
AU - Wylie-Rosett, J.
AU - Rohan, T.
AU - Hoover, D. R.
AU - Smoller, S.
AU - Burk, R. D.
AU - Yu, H.
PY - 2001
Y1 - 2001
N2 - Increasing evidence indicates that individuals with type 2 diabetes (diabetes) are at elevated risk for several common human malignancies, including cancers of the colon, breast, endometrium, pancreas, and liver. In particular, the consistent positive results reported by prospective investigations make it unlikely that methodologic issues, occult tumors, or chance results could explain the findings. Since diabetes and impaired fasting glucose together affect >25% of Americans above age 50, even a moderate etiologic association (e.g., relative risk = 1.5) would explain >10% of involved malignancies. Laboratory studies have suggested biologically plausible mechanisms. Insulin, for example, is typically at high levels during the development and early stages of diabetes. Activation of the insulin receptor by its ligand, or cross-activation of the insulin-like growth factor-I receptor, has been shown to be mitogenic and promote tumorigenesis in various model systems. A "unifying concept," in fact, holds that hyperinsulinemia may underlie the cancer associations of several additional risk factors, including high waist circumference, visceral fat, waist-to-hip ratio, body mass index, sedentary lifestyle, and energy intake. In this review, we assess current evidence regarding the relation of type 2 diabetes with cancer, and evaluate the findings in terms of well-accepted criteria for establishing causality.
AB - Increasing evidence indicates that individuals with type 2 diabetes (diabetes) are at elevated risk for several common human malignancies, including cancers of the colon, breast, endometrium, pancreas, and liver. In particular, the consistent positive results reported by prospective investigations make it unlikely that methodologic issues, occult tumors, or chance results could explain the findings. Since diabetes and impaired fasting glucose together affect >25% of Americans above age 50, even a moderate etiologic association (e.g., relative risk = 1.5) would explain >10% of involved malignancies. Laboratory studies have suggested biologically plausible mechanisms. Insulin, for example, is typically at high levels during the development and early stages of diabetes. Activation of the insulin receptor by its ligand, or cross-activation of the insulin-like growth factor-I receptor, has been shown to be mitogenic and promote tumorigenesis in various model systems. A "unifying concept," in fact, holds that hyperinsulinemia may underlie the cancer associations of several additional risk factors, including high waist circumference, visceral fat, waist-to-hip ratio, body mass index, sedentary lifestyle, and energy intake. In this review, we assess current evidence regarding the relation of type 2 diabetes with cancer, and evaluate the findings in terms of well-accepted criteria for establishing causality.
UR - http://www.scopus.com/inward/record.url?scp=0034947272&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0034947272&partnerID=8YFLogxK
U2 - 10.1089/152091501300209633
DO - 10.1089/152091501300209633
M3 - Review article
C2 - 11478333
AN - SCOPUS:0034947272
SN - 1520-9156
VL - 3
SP - 263
EP - 274
JO - Diabetes Technology and Therapeutics
JF - Diabetes Technology and Therapeutics
IS - 2
ER -