Aspirin;
Pancreatic cancer;
Cancer chemoprevention;
Cancer therapy;
Cancer microenvironment;
Cancer biology;
NONSTEROIDAL ANTIINFLAMMATORY DRUGS;
NF-KAPPA-B;
ACTIVATED PROTEIN-KINASE;
TUMOR-CELL REPOPULATION;
ENGINEERED MOUSE MODEL;
REGULATORY T-CELLS;
LOW-DOSE ASPIRIN;
COLORECTAL-CANCER;
PROSTAGLANDIN E-2;
IN-VIVO;
D O I:
10.1016/j.bbcan.2016.08.002
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
Pancreatic cancer is one of the most aggressive malignancies with dismal prognosis. Recently, aspirin has been found to be an effective chemopreventive agent for many solid tumors. However, the function of aspirin use in pancreatic cancer largely remains unknown. We herein argued that aspirin could also lower the risk of pancreatic cancer. Importantly, aspirin assumes pleiotropic effects by targeting multiple molecules. It could further target the unique tumor biology of pancreatic cancer and modify the cancer microenvironment, thus showing remarkable therapeutic potentials. Besides, aspirin could reverse the chemoradiation resistance by repressing tumor re population and exert synergistic potentials with metformin on pancreatic cancer chemoprevention. Moreover, aspirin secondarily benefits pancreatic cancer patients through modestly reducing cancer pain and the risk of venous thromboembolism. Furthermore, new aspirin derivatives and delivery systems might help to improve risk to -benefit ratio. In brief, aspirin is a promising chemopreventive agent and exerts significant therapeutic potentials in pancreatic cancer. (C) 2016 Elsevier B.V. All rights reserved.