AI Article Synopsis
- The text discusses mathematical models for two key mechanisms that helped multicellularity develop: how cells differentiate into various types (phenotype divergence) and how they cooperate with each other.
- It highlights how these mechanisms are altered in tumor cell populations, referencing the atavistic theory of cancer, which sees cancer as a phenomenon that arises from multicellular organisms.
- The study contrasts the emergence of multicellularity through evolutionary pressures and the organized development of multicellular organisms from a zygote, also exploring how cancer affects these processes, supported by insights from biology, mathematics, and philosophy of science.
Article Abstract
We discuss the mathematical modelling of two of the main mechanisms that pushed forward the emergence of multicellularity: phenotype divergence in cell differentiation and between-cell cooperation. In line with the atavistic theory of cancer, this disease being specific of multicellular animals, we set special emphasis on how both mechanisms appear to be reversed, however not totally impaired, rather hijacked, in tumour cell populations. Two settings are considered: the completely innovating, tinkering, situation of the emergence of multicellularity in the evolution of species, which we assume to be constrained by external pressure on the cell populations, and the completely planned-in the body plan-situation of the physiological construction of a developing multicellular animal from the zygote, or of bet hedging in tumours, assumed to be of clonal formation, although the body plan is largely-but not completely-lost in its constituting cells. We show how cancer impacts these two settings and we sketch mathematical models for them. We present here our contribution to the question at stake with a background from biology, from mathematics and from philosophy of science.
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| http://dx.doi.org/10.1093/imammb/dqae005 | DOI Listing |
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