Fig. 14

a, b, c Karyotypic evidence that the metastasis IGR-37 is an individual subspecies of melanoma IGR-39. The karyotypic theory of metastasis predicts that metastases have individual clonal karyotypes that differ from those of parental cancers in individual metastasis-specific aneusomies. To test this theory we have compared karyotype-arrays of the metastasis IGR-37 to that of the primary cancer IGR-39 prepared as described for Fig. 9. Figure 14 a, b , c and the attached table show that 55–100% of the chromosomes of the parental cancer IGR-39 and 50–100% of the chromosomes of the metastasis IGR-37 were clonal, and that cancer and metastasis formed similar clonal patterns. These patterns show, however, that metastasis coincided with a reduction in the ploidy of the parental cancer from hyper-tetraploid to hyper-triploid. Moreover, the karyotype of the metastasis differed from that of the primary cancer in about 27 of an average of 31 metastasis-specific aneusomies (Fig. 14 a, b, c and Table 1). Since the ploidy-shift changed the relative chromosome copy numbers of many aneusomies, the percentage of metastasis-specific aneusomies is, however, larger than if it were based on qualitative differences only (see Table 1). As in all other hyper-diploid cancers, the copy numbers of most non-clonal chromosomes including marker chromosomes differed from clonal averages ± 1 (Fig. 14 a, b and specifically Fig. 14c ). Again, the chromosomes with non-clonal copy numbers represent the ongoing karyotypic variation predicted by the inherent variability of cancer-specific aneuploidy (See Background). We conclude that the metastasis IGR-37 is a subspecies of the parental melanoma IGR-39