ABSTRACT

The chromosomal imbalance theory (Table 5.1) states that initiation of aneuploidy coupled with the autocatalyzed progression of aneuploidy during cell division is necessary and sufficient to generate cancer on the rare occasions the cells survive. If the progression of aneuploidy continues unabated, cancer cells result, which behave much like new unicellular “species” with unique, ever-changing karyotypes and phenotypes. Th e very low frequencies of carcinogenesis refl ect the very low probability of aneuploid cells acquiring reproductive autonomy-i.e. a new cellular species-by random karyotypic variations (Li et al. 2009). This mechanism explains the “conspicuously” long neoplastic

latencies of carcinogenesis (Cairns 1978, Pitot 2002, Rous 1967, Yamagiwa and Ichikawa 1915).