Table 1 |
|||
| The potential mechanisms of diabetes in PanCa | |||
| Parameters | Role in PanCa | Refs | |
| Pancreatic duct | Enlargement | Mechanical obstruction | [24] |
| Replication increased | Predisposing factor | [25] | |
| Hyperinsulinism and insulin resistance | Post-insulin receptor defect | Impaired glycogen synthesis and storage | [27] |
| Plasma glucagon levels and IAPP | Early development of PanCa | [28] | |
| Polymorphism of -23HphI (A/T) | Pathogenesis of PanCa | [29] | |
| Tumor size | Increased | Decreased postresection survival | [31] |
| Enhanced growth | [32] | ||
| Genetic variants | HK2 R844K GA/AA genotype | Increased risk | [33] |
| K-ras codon 12 mutations | Increased risk | [34] | |
IAPP, islet amyloid polypeptide; PanCa, pancreatic cancer.
Li et al. World Journal of Surgical Oncology 2012 10:171 doi:10.1186/1477-7819-10-171