Diabetes and pancreatic cancer

被引:122
作者
Cui, YunFeng [1 ,2 ]
Andersen, Dana K. [1 ]
机构
[1] Johns Hopkins Univ, Sch Med, Dept Surg, Johns Hopkins Bayview Med Ctr, Baltimore, MD 21205 USA
[2] Tianjin Med Univ, Tianjin Nankai Hosp, Nankai Clin Sch Med, Dept Surg, Tianjin, Peoples R China
关键词
POPULATION-BASED COHORT; ISLET AMYLOID POLYPEPTIDE; BODY-MASS INDEX; INSULIN-RESISTANCE; CELL-PROLIFERATION; DUODENAL HOMEOBOX-1; GLUCOSE-TOLERANCE; BARIATRIC SURGERY; FECAL ELASTASE-1; EARLY-DIAGNOSIS;
D O I
10.1530/ERC-12-0105
中图分类号
R73 [肿瘤学];
学科分类号
100214 [肿瘤学];
摘要
Epidemiological studies clearly indicate that the risk of pancreatic cancer (PC) is increased in diabetic patients, but most studies focus on overall diabetes or type 2 diabetes mellitus (T2DM), and there are few studies on the risks of type 1 and type 3c (secondary) diabetes. Possible mechanisms for increased cancer risk in diabetes include cellular proliferative effects of hyperglycemia, hyperinsulinemia, and abnormalities in insulin/IGF receptor pathways. Recently, insulin and insulin secretagogues have been observed to increase the PC risk, while metformin treatment reduces the cancer risk in diabetic subjects. In addition, anticancer drugs used to treat PC may either cause diabetes or worsen coexisting diabetes. T3cDM has emerged as a major subset of diabetes and may have the highest risk of pancreatic carcinoma especially in patients with chronic pancreatitis. T3cDM is also a consequence of PC in at least 30% of patients. Distinguishing T3cDM from the more prevalent T2DM among new-onset diabetic patients can be aided by an assessment of clinical features and confirmed by finding a deficiency in postprandial pancreatic polypeptide release. In conclusion, diabetes and PC have a complex relationship that requires more clinical attention. The risk of developing PC can be reduced by aggressive prevention and treatment of T2DM and obesity and the prompt diagnosis of T3cDM may allow detection of a tumor at a potentially curable stage. Endocrine-Related Cancer (2012) 19 F9-F26
引用
收藏
页码:F9 / F26
页数:18
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