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Fig. 15 | Molecular Cytogenetics

Fig. 15

From: Inherent variability of cancer-specific aneuploidy generates metastases

Fig. 15

a, b, c, d Karyotypic evidence that the metastases A13-A and A13-D are individual subspecies of the pancreatic cancer A-13B. 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 the karyotype-arrays of the metastases A13-A and A13-D to that of the primary cancer A-3B. The karyotype arrays were again prepared as described for Fig. 9. Figure 15 a, b , c and the attached table show that the chromosomes of the cancer were 55–95% clonal and that of the chromosomes of metastasis A13-A were 75–100% and those of metastasis A13-D were 75–100% clonal, and that all three cancers formed related clonal patterns. As shown in Table 1, the karyotype of the metastasis A13-A differed from that of the primary cancer A13-B in 27 of 49 aneusomies and metastasis A13-D differed from that of the primary in 16 of 49 aneusomies (Fig. 15 a, b, c, d). The copy numbers of most non-clonal chromosomes including marker chromosomes differed from clonal averages ± 1 (Fig. 15 a, b , c and specifically Fig. 15d ). 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 metastases A13-A and D are subspecies of the parental pancreatic cancer A13-B

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