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. 2019 Sep 20;10:892. doi: 10.3389/fgene.2019.00892

Figure 1.

Figure 1

Theoretical model for CIN mediating (A) cancer and (B) neurodegeneration. (A) Genetic defects and genetic-environmental interactions may cause chromosomal/genomic changes, which produce CIN; alternatively, cell populations may adapt to aneuploidy and CIN evolving to a cell population with a fitness advantage. Cells affected by CIN and tolerating deteriorating effects of CIN on cellular homeostasis are able to evolve clonally to produce malignancy. (B) CIN/somatic mosaicism affecting a significant proportion of cells interacting with environmental triggers may result into progressive neuronal cell loss (neurodegeneration) under natural selection pressure and through the programmed cell death (N, normal neurons; CIN, neuronal cell affected by CIN). The model is based on the observations of CIN in the neurodegenerating brain and cancers (Iourov et al., 2009a; Iourov et al., 2009b; Arendt et al., 2010; Granic et al., 2010; Iourov et al., 2011; Jeppesen et al., 2011; Yurov et al., 2011; Driver, 2012; Kennedy et al., 2012; Vijg, 2014; Yurov et al., 2014; Bajic et al., 2015; Heng, 2015; Arendt et al., 2017; Rangel et al., 2017; Caneus et al., 2018; Leija-Salazar et al., 2018; Yurov et al., 2018; Machiela, 2019; Simonetti et al., 2019).