436 1 GENETICS OF SOMATIC CELLS 



to exclude the possibility that resistance against methylcholanthrene-induced sarcomas 

 in mice, previously demonstrated by Foley, 383 was caused by residual heterozygosis 

 in the inbred strains used. They have demonstrated that normal tissues from the very 

 same mouse in which the neoplasm had been originally induced could not immunize 

 against the tumor; neither could implants of methylcholanthrene-induced tumor 

 tissue immunize isologous mice against skin grafts taken from the same animal in which 

 the tumor had arisen originally. Resistance against a given methylcholanthrene- 

 induced sarcoma was not necessarily accompanied by cross resistance against another 

 one, induced in the same fashion and in the same strain, although there was evidence of 

 incomplete cross reaction between certain tumors; thus the different tumors tended to 

 be immunologically distinct. 



Revesz 1050 has confirmed the findings of Prehn and Main. He has also shown 

 that no similar resistance could be induced against lymphomas of recent origin. On 

 the other hand, with two lymphomas and one carcinoma of inbred strains that have 

 been kept in serial transplantation through several years, a state of incompatibility 

 could be readily demonstrated after the same pretreatment, apparently as a result of 

 the isoantigenic differences that are known to develop between sublines of mice carried 

 independently and therefore necessarily also between a line of inbred mice and its 

 transplanted tumor carried in serial passage through long periods of time. 



These experiments made it highly improbable that the resistance against methyl- 

 cholanthrene-induced sarcomas was due to residual heterozygosis of the inbred strains, 

 since such heterozygosis could only explain the results if it would exert a differential 

 effect on the compatibility of methylcholanthrene-induced sarcoma cells on the one 

 hand, and spontaneous sarcomas, carcinomas, lymphomas, and skin on the other 

 hand. A last trace of doubt did nevertheless remain, particularly since there were 

 data to indicate that different tissues may respond differently to weak differences in 

 histocompatibility. 789 ' 1396 The final proof was obtained when it was demonstrated 

 that resistance can also be built up in the primary autochthonous host from which the 

 tumor had been excised. 727 The autochthonous hosts operated on, together with 

 groups of isologous animals, were pretreated with irradiated sarcoma cells and subse- 

 quently challenged with increasing doses of viable cells. Untreated isologous controls 

 were inoculated with the same doses of cells at the same time. Resistance could be 

 demonstrated with 12 out of 16 tumors in the autochthonous and 19 out of 22 tumors 

 in the isologous hosts. Resistance was relative rather than absolute, and it broke down 

 when the dose of viable cells was progressively increased. Resistance against a given 

 sarcoma did not lead to cross resistance against a different sarcoma induced by methyl- 

 cholanthrene in the same genotype. Repeated inoculation of homologous, MC-induced 

 sarcoma tissue prior to injection of carcinogen did not reduce the yield of primary 

 sarcomas. 



Perhaps the most unexpected among these findings was the individually different 

 antigenicity of the MC-induced sarcomas. This cannot be explained satisfactorily 

 at the present time, although it does indicate a cytogenetic individuality of the different 



