Gastric cancer is the third leading cause of cancer-related mortality worldwide. This is in part due to the asymptomatic nature of the disease, which often results in late-stage diagnosis, at which point there are limited treatment options. Even when treated successfully, gastric cancer patients have a high risk of tumor recurrence and acquired drug resistance. It is vital to gain a better understanding of the molecular mechanisms underlying gastric cancer pathogenesis to facilitate the design of new-targeted therapies that may improve patient survival. A number of chemically and genetically engineered mouse models of gastric cancer have provided significant insight into the contribution of genetic and environmental factors to disease onset and progression. This review outlines the strengths and limitations of current mouse models of gastric cancer and their relevance to the pre-clinical development of new therapeutics.
Funding
The work in the laboratory of T.L.P. is supported by the Victorian State Government Operational Infrastructure Support and the National Health and Medical Research Council Australia (NHMRC) project grants nos. 1008614, and 1080498, Cancer Australia project grant no. 1407672, and Worldwide Cancer Research project grant no. 14-1197. The work in the laboratory of M. E. is supported by Ludwig Cancer Research, the Victorian State Government Operational Infrastructure Support, the IRIISS scheme of the NHMRC, and NHMRC project grants nos. 1069024, 1067244, and 1092788. A. R. P. is supported by an Australian Post Graduate Award (APA) and a Cancer Therapeutics CRC (Ctx) PhD Top-Up Scholarship. R. O'D received project grant support from NHMRC no. 1025239 and the Victorian Cancer Agency no. ECSG13014.