Many have land, if only small plots after generations of division among sons.
Furthermore, since a gland can never exceed the fixed total number of cells, non-CSCs can never undergo more than 12 generations of division (see Table 1).
However for several generations of division postexposure, they begin to show high levels of nonclonal cytogenetic aberrations and reproductive failure.
We simulate data for tumors having different growth rates, models for cell division, and numbers of cancer stem cells (CSCs) at various stages of their development (numbers of generations of cell division) and plot the average estimates for the three different epigenetic distances: between half (BH), within half (WH) and within gland (WG) for various parameter settings (Figure 6).
The LAB E. coli shuttle vector was constructed by ligating pCB42 and pEK104, and the resulting shuttle vector, pLeuCM42, showed a high segregational stability in L. citreum CB2567 after 100 generations of cell division.
In these types of models, the estimates of DNA methylation copy errors and the total number of generations of cell division are not identifiable.
A stem cell produces a progenitor cell committed to proliferation, resulting in a clone with hundreds of descendant cells through many generations of cell division.
Furthermore, supposedly identical clonal cell populations have been shown to deviate in their genetic expression [3] and response to environmental stimuli [4] over generations of cell division.
Focusing first on the estimate of BH distance and comparing results in the right column to results in the left column, we see that the BH distance is higher at 700 generations of cell division than at 100 generations.
We simulate 100, 400, and 700 generations of cell division in each tumor half under the probabilistic survival model, fixing the number of CSCs per gland at 128 and 1024.
This suggests that a slower Gompertzian growth rate cannot account for the larger BH-WH distances that we observe in four of our tumors (differences = 0.47, 0.68, 0.80, 1.63), and motivates us to explore whether asymmetric growth, where one tumor half undergoes more generations of cell division than the other, could explain such differences.
