428 GENETICS OF SOMATIC CELLS 



including methylcholanthrene-induced sarcomas, spontaneous and estrogen-induced 

 mammary carcinomas, spontaneous and estrogen-induced lymphomas, and estrogen- 

 induced and dependent testicular tumors. 545, 716, 717, 722, 724 Clear-cut isoantigenic 

 variants could be extracted from a number of tumors by utilizing the homograft 

 reaction of coisogenic resistant hosts as selective force. All tumors tested were at the 

 primary stage or in their earliest transfer generations. They showed different types of 

 behavior when tested in the parental strains or in foreign genotypes. A few were 

 nonspecific, either immediately upon their origin or after a certain number of serial 

 passages. They grew indiscriminately in both parental types and also in foreign strains. 

 They grew less well or not at all in mice of the parental strains if these had been pre- 

 immunized against the isoantigens of the opposite parent or in foreign genotypes 

 preimmunized against the hybrid genotypes of the tumor. 



The great majority of the tumors tested were highly specific in their transplantation 

 behavior and grew regularly in the F 1 hybrid genotype of origin, but only seldom or not 

 at all in any of the parental strains. Occasional takes in mice of parental strains 

 were of great potential interest for this study, and such tumors were regularly tested 

 by further transplantation into both parental strains and into the other two coisogenic 

 resistant lines as well, together with various F 1 combinations between these and the 

 two parents. Different types of behavior could be observed. Some tumors failed to 

 grow upon repeated testing in the same parental genotype in which they appeared. 

 Others grew in a certain, often high, proportion of the same parental strain but not 

 in the other parent or in foreign genotypes. Tests in preimmunized mice gave interest- 

 ing results. Some variants were fully compatible with their new parental host even if 

 preimmunized by one or several inoculations of normal or malignant tissues from the 

 opposite parental strain. Others grew only in nonimmunized mice and regressed in 

 preimmunized animals. When lines of the latter type were carried in nonimmunized 

 hosts of the parental strain during a series of transfers, one of two alternatives could 

 happen: the line died out after a number of passages, failing to take even in non- 

 immunized hosts, or it became increasingly and sometimes fully compatible with 

 preimmunized hosts. The latter development was observed repeatedly with certain 

 host-tumor combinations. 722 



Occasional takes were sometimes obtained in coisogenic, resistant mice outside 

 the two parental strains (for example, with A x A.SW F x tumors in A. BY or A. CA 

 mice or in various F 1 hybrids derived from crosses between A. BY or A.CA and one of 

 the parental strains) . In spite of extensive testings, it was never possible to establish 

 a subline that would breed true in these partially foreign genotypes. Upon repeated 

 testing, they either refused to grow at all, or turned out to be nonspecific and grew in a 

 wide variety of strains, as the tumors did that were nonspecific from the beginning. 

 Even in this case, growth in foreign genotypes could usually be prevented by previous 

 immunization. 



A series of similar tests were performed with tumors induced in an identical 

 fashion in homozygous mice of the strains A, A . SW, or A . CA. Takes were much less 



