We also assessed the potential effects of veterinary drugs on embryo damage and immunodepression increasing the probability of acquisition and proliferation of pathogens causing fatal disease [6], [10] [12], [21].
Specifically, model results indicated that the probability of CSC symmetric proliferation is responsible of a switching-like behavior which discriminates between tumorigenesis and unsustainable tumor growth.
Applying our methodology to this model we found that the probability of CSC symmetric proliferation is responsible for a switching-like behavior.
At the existence of coral microparticles, by increase in open porosity of the scaffolds, the probability of cell diffusion enhanced, as such the proliferation rate and ultimate viable cells on the related rolls increased as a result of increased area for cell growth.
The resulting proliferation could increase the probability of mistakes being made in DNA replication and setting these mistakes as mutations.
Many potentially harmful mutations, however, increase the probability of triggering apoptosis and, hence, initially lead to cells with reduced net proliferation rates.
In addition, since proliferation is induced by VEGF (Gerhardt et al. 2003), we could improve the model not only by restricting proliferation to stalk cells, but also by increasing the probability of cell division with higher VEGF concentrations.
As LOH is mainly caused by mitotic recombination, the probability of LOH events is dependent on the number of clonal generations during asexual proliferation.
