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In this article the authors introduce the concept of a "diversification factor", which is probably the key issue of the article.
Finally, we emphasize that validation of the hypothesis that stem cells can adapt their aneuploidy rate through a diversification factor would have significant therapeutical implications, when specialized to cancer stem cells.
Such refined ability is unlikely to be the product of a single, specific tumor evolutionary history, rather, we will argue that embryo and adult stem cells already display very finely regulated rates of aneuploidy, suggesting that a common cellular mechanism of adaptation of aneuploidy is at play, a diversification factor, which is possibly reactivated in cancer stem cells.
We also discuss the potential origin of this self-regulatory ability in the wider context of developmental and comparative biology and we hypothesize the existence of a diversification factor, i.e. a cellular mechanism that regulates adaptation of aneuploidy rates, active in all embryo, adult and cancer stem cells.
And this brings us to the proposition we stated in the introduction on adaptive aneuploidy in cancer cells: in light of the refined use of aneuploidy in stem cells, self-regulation of aneuploidy as argued in this Discussion could be a reactivation, in cancer stem cells, of a preexisting cellular mechanism common to embryo and adult stem cells - a diversification factor.
Finally, they discuss the potential origin of this self-regulatory ability in the wider context of developmental and comparative biology with emphasis on a putative "diversification factor", defined as a cellular mechanism regulating the adaptation of aneuploidy rates, which is active in all embryonic and adult cells, as well as cancer stem cells.
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Using the topological imbalances and the time line we discuss the potential role of different diversification factors that might have shaped the rodents radiation.
For example, the category technology diversification included factors related to technologies and libraries supported by the components associated with the given vulnerability.
However, the complete ablation of CIB1 in DT40 or mice demonstrated that this protein is dispensable for both IGC and CSR in these organisms (i.e., CIB1 is not an antibody diversification co-factor).
Further studies will be needed to clarify the relation between gene diversification and external factors in organisms' environments.
The relationship between these two modes of functional diversification of transcription factor paralogs has not been previously investigated, and is essential for understanding adaptive evolution of transcription factor gene families.
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