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How the growth rate of host cells affects cancer risk in a deterministic way.

Clément DraghiLouise VigerFabrice DenisChristophe Letellier
Published in: Chaos (Woodbury, N.Y.) (2018)
It is well known that cancers are significantly more often encountered in some tissues than in other ones. In this paper, by using a deterministic model describing the interactions between host, effector immune and tumor cells at the tissue level, we show that this can be explained by the dependency of tumor growth on parameter values characterizing the type as well as the state of the tissue considered due to the "way of life" (environmental factors, food consumption, drinking or smoking habits, etc.). Our approach is purely deterministic and, consequently, the strong correlation (r = 0.99) between the number of detectable growing tumors and the growth rate of cells from the nesting tissue can be explained without evoking random mutation arising during DNA replications in nonmalignant cells or "bad luck". Strategies to limit the mortality induced by cancer could therefore be well based on improving the way of life, that is, by better preserving the tissue where mutant cells randomly arise.
Keyphrases
  • induced apoptosis
  • cell cycle arrest
  • endoplasmic reticulum stress
  • gene expression
  • cell death
  • immune response
  • climate change
  • papillary thyroid
  • smoking cessation
  • squamous cell