Phenotype divergence and cooperation in isogenic multicellularity and in cancer

We discuss the mathematical modelling of two of the main mechanisms which pushed forward the emergence of multicellularity: phenotype divergence in cell differentiation, and between-cell cooperation. In line with the atavistic theory of cancer, a disease that is 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 evolutionary emergence of multicellularity, 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 (fecundated egg), 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.
This is joint work with Frank Ernesto Alvarez Borges, La Habana and Paris Dauphine Universities, on leave from INSA Toulouse.
References: 1. Alvarez, F.E., Clairambault, J. Phenotype divergence and cooperation in isogenic multicellularity and in cancer (authors' preprint, June 2023), https://hal.science/hal-04145070. In revision, January 2024
2. Alvarez, F. E., Carrillo, J. A., Clairambault, J. Evolution of a structured cell population endowed with plasticity of traits under constraints on and between the traits. (authors' preprint), https://hal.science/hal-03344894. J Math Biol, 85:64, September 2022