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Fig. 1 | Molecular Cytogenetics

Fig. 1

From: Inherent variability of cancer-specific aneuploidy generates metastases

Fig. 1

Karyotypic theory of metastasis. According to the karyotypic theory mutagenic and non-mutagenic carcinogens induce random aneuploidy in normal cells at carcinogen-dependent rates, r1. Aneuploidy then auto-catalyzes further random karyotypic variation, because it unbalances thousands of genes including mitosis-genes at aneuploidy-dependent rates, r2. Most such random variants perish. Rare karyotypic variants, however, form new autonomous cancer species with near-diploid, hypo-diploid or hyper-diploid karyotypes at very low rates, r3, because the probability to form a new autonomous cell is very low [7577, 104, 105, 109, 135]. Owing to the inherent instability of aneuploidy, the karyotypes of new cancer species vary at aneuploidy-dependent rates, r2, within margins that are defined by selection for cancer-specific autonomy. As a result of this inherent variability of cancer karyotypes, new autonomous karyotypic subspecies with metastatic phenotypes arise stochastically. Since the probability of forming new autonomous subspecies by random variation of cancer karyotypes is very low – as in conventional subspeciation – metastases would occur typically at low rates, r4, such as the 10^-8 per-cell rate described in the Background in reference [9]. These rates are still higher than those of carcinogenesis from normal cells, r3 [136]. The Figure also records graphically our results that the karyotypic complexity of cancers is highly conserved in metastases. Thus hyper-triploid cancers formed hyper-triploid metastases and near-diploid cancers formed near-diploid metastases. There was no evidence of spontaneous alterations of the clonal karyotypic complexity of cancers or metastases; hence ‘r?’ in Fig. 1

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