GENETICS OF SOMATIC CELLS 429 



frequently obtained with such tumors in coisogenic resistant mice carrying foreign 

 H-2 alleles than was the case when heterozygous F 1 tumors were tested in one parental 

 strain. Whenever such occasional takes were obtained, they failed to breed true in 

 the new genotype and either died out after one or a few passages, or showed a highly 

 nonspecific behavior. 716 



This experience with homozygous and heterozygous tumors indicated that we 

 were dealing with at least two different phenomena. One probably corresponds to 

 what Snell describes as false positives, when the tumor grows in the presence of and in 

 spite of a homograft reaction, and when its growth can be at least partially prevented 

 by testing it in preimmunized hosts. 1237, 1239 This result is not particularly frequent 

 on the whole, and the liability of its occurrence varies from tumor to tumor. It may 

 occur with both homozygous and heterozygous tumors and also with the selected and 

 originally specific sublines of the latter. It does not seem to be limited to the parental 

 strains or to certain specific genotypes, although it may be obtained with greater ease 

 in one genotype than in another. The latter variation may be attributed to variations 

 in the strength of the homograft reaction, depending on the nature of the isoantigenic 

 barrier between tumor and host. 



The appearance of variants, selectively compatible with one of the parental strains, 

 appears to be a different phenomenon, for the following reasons. A certain percentage 

 of takes was obtained in one of the parental strains. When tested further, some of these 

 tumors were selectively compatible with the parental strain in question but not with the 

 opposite parent or any other strain. They grew in preimmunized mice of their new 

 strain to a varying extent, but in a number of cases they were compatible even with 

 such hosts, either immediately or after one or a few passages in nonimmunized mice. 

 From certain tumors it was possible to establish both kinds of variants, selectively 

 compatible with the maternal or the paternal strain, respectively, but still refusing to 

 grow in the opposite parent. This result could only be obtained with heterozygous 

 tumors and selective compatibility was restricted to the parental strains, excluding other 

 coisogenic resistant mice carrying foreign alleles at the H-2 locus, and semi-isologous 

 F x hybrids differing from the genotype of origin with regard to one substitution at the 

 H-2 locus. 



The question arose whether such selectively compatible variants grow in their 

 parental hosts because they have lost the specific isoantigenicity determined by the 

 H-2 factor derived from the opposite parental strain. This was tested in a number of 

 different ways. The original tumor and its variant(s) were compared 64, 717, 724 for 

 their ability to induce the formation of hemagglutinins 459 and cytotoxic antibodies 460 

 directed specifically against the //-2-determined isoantigenic products of both parental 

 strains, for their ability to absorb preformed hemagglutinins or cytotoxic antibodies 

 from isoimmune sera, and for their ability to provoke a second-set response subsequent 

 to the inoculation of heavily irradiated cells into the variant-compatible type (tested 

 by challenging the pretreated mice with another F^hybrid tumor derived from the 

 same genotype and capable of temporary growth in the parental type in question) . 



