2013/03/26 by Domenico Napoletani, Napoletani, Domenico, Michele Signore +3
Agricultural and Biological Sciences · Biochemistry, Genetics and Molecular Biology · #Cancer Genomics and Diagnostics #Cell Behavior (q-bio.CB) #Chromosomal and Genetic Variations #FOS: Biological sciences #Genomics (q-bio.GN) #Genomics and Rare Diseases
paper · pdf · doi:10.48550/arxiv.1303.6374
openalex publication_date 2013/03/26 · openalex created_date 2025/10/10 · openalex updated_date 2026/08/01
We analyze and reinterpret experimental evidence from the literature to argue for an ability of tumor cells to self-regulate their aneuploidy rate. We conjecture that this ability is mediated by a diversification factor that exploits molecular mechanisms common to embryo stem cells and, to a lesser extent, adult stem cells, that is eventually reactivated in tumor cells. Moreover, we propose a direct use of the quasispecies model to cancer cells based on their significant genomic instability (i.e. aneuploidy rate), by defining master sequences lengths as the sum of all copy numbers of physically distinct whole and fragmented chromosomes. We compute an approximate error threshold such that any aneuploidy rate larger than the threshold would lead to a loss of fitness of a tumor population, and we confirm that highly aneuploid cancer populations already function with aneuploidy rates close to the estimated threshold.