13 



and intrepretations were complicated by variation in 

 technique and cell lines. Using low temperature conditions, 

 Noonan and Burger (1973a) were able to demonstrate that in 

 the absence of endocytosis and with appropriate corrections 

 for surface area and volume differences, certain virally 

 transformed cells possessed 3 to 5 times the number of Con 

 A binding sites of a normal cell. Similar results were 

 obtained with normal cells at mitosis (Noonan et al., 1973), 

 after brief protease treatment (Noonan and Burger, 1973b) or 

 exposure of certain cell lines to dibutyrylcyclic AMP (Veen 

 et al., 1976). Under these conditions slight differences 

 in the numbers of Con A binding sites could be detected. 

 Although the relationship of the Con A binding to increased 

 agglutinability or the transformed state still remains 

 undetermined, the altered surface structure of transformed 

 cells may allow for differential interaction with Con A- 

 inhibitor conjugates in comparison to normal cells. Kitao 

 and Hattori (1977) tested a conjugate of Con A and dauno- 

 mycin for its ability to suppress the in vivo development 

 of Ehrlich ascites and L1210 cells. Prolonged survival 

 of the host in comparison to free daunomycin was obtained 

 following administration of the conjugate with either cell 

 type. While characterization of this conjugate was minimal 

 and the test results qualitative in nature, selective toxi- 

 city of Con A conjugates was implied. The use of Con A 

 as a targeting agent would therefore seem feasible based 

 on the known differences between cells with respect to 



