Abstract
The golden Syrian hamster (Mesocricetus auratus) has long been a valuable rodent model of human diseases, especially infectious and metabolic diseases. Hamsters have also been valuable models of several chemically induced cancers such as the DMBA-induced oral cheek pouch cancer model. Recently, with the application of CRISPR/Cas9 genetic engineering technology, hamsters can now be gene targeted as readily as mouse models. This review describes the phenotypes of three gene-targeted knockout (KO) hamster cancer models, TP53, KCNQ1, and IL2RG. Notably, these hamster models demonstrate cancer phenotypes not observed in mouse KOs. In some cases, the cancers that arise in the KO hamster are similar to cancers that arise in humans, in contrast with KO mice that do not develop the cancers. An example is the development of aggressive acute myelogenous leukemia (AML) in TP53 KO hamsters. The review also presents a discussion of the relative strengths and weaknesses of mouse cancer models and hamster cancer models and argues that there are no perfect rodent models of cancer and that the genetically engineered hamster cancer models can complement mouse models and expand the suite of animal cancer models available for the development of new cancer therapies.