Abstract
Previous studies on isoantigenic variation in heterozygous mouse tumors have shown that cells with genetic information controlling H-2 antigens D and K in the cis position, i.e., on the same chromosome, did not give rise to D−K+ variants, while D−K− and D+K− variants were readily obtained. This was tentatively attributed to a chromosomal mechanism involving either deletion or, more probably, somatic crossing over. Another explanation that could not be excluded, however, was that D is a precursor of K. In the present work, neoplasms were studied that contained the genetic determinants for the same two antigens on two different homologous chromosomes, i.e., in the trans position. In this situation, the previously missing D−K+ variants were readily obtained. This makes the precursor hypothesis less probable and strengthens the postulate that the formation of isoantigenic variants has a chromosomal mechanism.