Fig. 1

Karyotypic theory of SV40 virus-induced neoplastic transformation. The karyotypic theory proposes that SV40 initiates carcinogenesis indirectly by inducing in infected cells preneoplastic aneuploidies at high rates (m1, in Fig. 1). Since aneuploidy destabilizes the karyotype by unbalancing thousands of genes, it catalyzes chain reactions of karyotypic and transcriptomic evolutions, also at high rates (m2, in Fig. 1). Eventually rare karyotypes evolve that encode cancer-specific autonomy of growth, at very low rates (m3, Fig. 1). The low probability of forming new autonomous cancer-species by random karyotypic and transcriptomic variations predicts the individuality of cancers. Although cancer karyotypes are congenitally aneuploid and thus unstable, they are stabilized or immortalized by selection for variants with cancer-specific autonomy. Owing to these inherent variations cancer karyotypes are heterogeneous within clonal margins (shaded in Fig. 1) [100–102]. The resulting spreads of quasi-clonal karyotypes are defined by ‘karyotype arrays’ in which multiple individual karyotypes of the same cancers are compared (shown below in Figs. 5, 6, 7, 11, 12, 13, 16 and 17)