THE CONTROL OF CELL RELATIONS 



Green (1954, 1957) has strongly supported the theory that 

 the essential lesion in the cancer cell is a loss of specific anti- 

 gens and that these, serving as identity markers, may play 

 a major part in maintaining normal cell relations. There is 

 much evidence to indicate that, with the development of 

 malignant change under the action of a chemical carcinogen, 

 the cells lose a component to which the carcinogen is specifi- 

 cally bound. This may be associated with loss of some anti- 

 genic specificity or even with the gain of a new antigenic 

 determinant. There is a real possibihty that such changes 

 may be associated with loss of the proximity control we have 

 been discussing. The only question is whether it is in the long 

 run more profitable to look at the immunological change as 

 a consequence of somatic mutation or to assume that immuno- 

 logical reactions enforce a specific type of somatic mutation. 

 In line with our general approach in these lectures, we should 

 prefer the first alternative. 



Green's (1957) assumption that, because cancer cells have 

 lost identity proteins they can produce antibody against 

 normal body cells which have retained them, is quite out of 

 accord with the clonal selection point of view. The appear- 

 ance in a proportion of cancer cases of serum changes, 

 including various types of globulin instability, increased 

 hexosamine, etc. and a rather low-grade direct Coombs test, 

 is best interpreted as due to the leakage of cell components 

 from the mahgnant tumour into the body fluids rather than 

 an auto-antibody reaction. Many suggestions have been 

 made that some human tumours provoke antibodies which 

 have an inhibitory action against their growth. Black, Opler 

 and Speer (1954) found that the prognosis was much better 

 if a resected gastric carcinoma showed an active lymphocytic 

 and plasma-cell reaction around the mahgnant cells than if 

 this was absent. It is reasonable to beheve that in such 

 tumours the mutations responsible had produced antigenic 

 determinants new to the body and that a homograft-type 

 immune response was in progress. 



195 13-2 



