Figure 1.

The speciation theory of cancer: Carcinogenesis in one stochastic karyotypic step. The speciation theory postulates that carcinogens or spontaneous accidents induce aneuploidy, i.e., losses or gains of chromosomes at dose-dependent rates, termed m1. By unbalancing chromosomes and thus mitosis genes aneuploidy initiates chain reactions of automatic karyotypic evolutions at aneuploidy-dependent rates, termed m2. Most such evolutions end with non-viable karyotypes, but a few become new cancer karyotypes at very low rates, termed m3 – in one stochastic step, as non-autonomous precursors are too unstable to accumulate. Because of its congenital “aneuploidy” (relative to normal) the cancer karyotype is variable at m2-rates, but is stabilized by clonal selection for autonomy within cancer-specific margins. Since aneuploidy changes the normal phenotype (squares), aneuploid cells are shown as half round-half squares and cancer cells are shown as circles.