The link between pancreatic cancer (PC) and diabetes mellitus is recognized, however
controversy still exists because no criteria have been established for the efficient
selection of a high-risk group among patients with diabetes mellitus. Regulation of
endocrine cell mass is thought to have a central role in the pathogenesis of both diseases.
The processes that operate during pancreatic adaptation to a changing hormonal
milieu are important in pancreatic carcinogenesis. There is evidence that
somatostatin and its receptors are fundamental regulators of endocrine cell mass and
are involved in islet tumorigenesis [57].
A hospital-based case-control study revealed that cigarette smoking, family history
of PC, heavy alcohol consumption (60 ml ethanol/day) and diabetes mellitus
are significant risk factors for PC. The significant synergy between these risk factors
suggests a common pathway for carcinogenesis of the pancreas [58].
Because of the poorly understood temporal association between diabetes mellitus
and PC, a research group at the Mayo Clinic College of Medicine, Rochester,
Minn., USA [59] compared temporal patterns in diabetes prevalence in PC and
controls. Diabetes has a high prevalence in PC and frequently is now onset.
Longstanding type 2 diabetes increases the risk of PC by approximately 50%.
Furthermore, there seems to be a positive association between obesity and PC [60].
However, as the mechanisms for these associations remain speculative, further
studies are deserved. Above all, there is an urgent need for the identification of
specific biomarkers for PC-induced diabetes, which may allow screening for PC in
new-onset diabetes.
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