ABSTRACT
While murine analogs of some members of the CEA gene family have been identified, such as biliary glycoprotein (Beauchemin et al., 1989; Huang et al., 1990; McCuaig et al., 1993; Robbins et al., 1991), no true CEA homolog has been identified in mice or rats to date (McCuaig et al., 1993). CEA-producing human tumor xenografts in immunocompromised animals have been widely used for testing CEAbased detection and therapeutic strategies, although these models have certain disadvantages (Sharkey et al., 1991). Several groups have developed rodent colon carcinomas expressing CEA through gene transfer to circumvent some of the limitations with other animal models (Pélegrin et al., 1992; Robbins et al., 1991). However, CEA-expressing rodent tumors propagated in immunocompetent mice also appear to have distinct disadvantages. Pélegrin et al. (1992) described the growth of several CEA transfected rat colon carcinoma lines, and found that the CEApositive cell lines grew at a slower rate than nontransfected cells. Some of the highest CEA expressers were also rejected. Similarly, Hand et al. (1993) showed that a CEAtransfected murine colon carcinoma cell line, MC-38, grew more slowly than the non-transfected parental tumor. In addition, complete tumor takes were not obtained even when a large number of cells were injected. The differences between their CEA-positive and non-transfected parental lines are presumably due to the expression of the antigenic human CEA molecule.
