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Metastasis as supra-cellular selection? A reply to Lean and Plutynski

The Original Article was published on 30 November 2015

The Original Article was published on 04 August 2012

Abstract

In response to Germain (Biol Philos 27:785–810, 2012. doi:10.1007/s10539-012-9334-2) argument that evolution by natural selection has a limited explanatory power in cancer, Lean and Plutynski (Biol Philos 31:39–57, 2016. doi:10.1007/s10539-015-9511-1) have recently argued that many adaptations in cancer only make sense at the tumor level, and that cancer progression mirrors the major evolutionary transitions. While we agree that selection could potentially act at various levels of organization in cancers, we argue that tumor-level selection (MLS2) is unlikely to actually play a relevant role in our understanding of the somatic evolution of human cancers.

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Notes

  1. Keeping in mind that contrary to MLS2, MLS1 is in many respects reducible to single-level selection (Kerr and Godfrey-Smith 2002).

  2. Another criticism made to the arguments from Germain (2012) was that "Whether or not a trait is due to a single mutation of large effect or many mutations of small effect is irrelevant to whether it is in fact an adaptation" (p. 53). We would like to correct here a possible misunderstanding of the original argument, which was that natural selection has more relevance for the explanation of those adaptations that are coherent accumulation of iterative changes, because these complex adaptations are proportionally more dependent on variations in the environment (versus variations in the initial architecture of the organism), than simple adaptations. This can also be framed following the distinction between “distribution explanation” and “origin explanation” by natural selection used by Godfrey-Smith (2009, p. 42–43): complex adaptations are those traits whose origin (rather than mere spread) itself must be explained by natural selection. This distinction is important to have in mind because this article also relies on it.

  3. Beyond the clinic, there are some very specific contexts where these limitations might not apply. The recent epidemy of transmissible cancer in Tasmanian devils (Murchison et al. 2012; Epstein et al. 2016) and the much older canine venereal cancer (Murgia et al. 2006) both show traces of evolution by natural selection escaping the lifespan of individual organisms. So far, only clonal cell-level evolutionary dynamics have been described in these systems, but if MLS2 was to be found anywhere in cancer, these cancers would be the first places to look.

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Correspondence to Pierre-Luc Germain.

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Germain, PL., Laplane, L. Metastasis as supra-cellular selection? A reply to Lean and Plutynski. Biol Philos 32, 281–287 (2017). https://doi.org/10.1007/s10539-016-9555-x

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Keywords

  • Cancer
  • Natural selection
  • Metastasis
  • Darwinian populations
  • Multi-level selection