%0 Book Section
%9 OS CH : Chapitres d'ouvrages scientifiques
%A Thomas, F.
%A Ujvari, B.
%A Gidoin, C.
%A Tasiemski, A.
%A Ewald, P.W.
%A Roche, Benjamin
%T Toward an ultimate explanation of intratumor heterogeneity
%B Ecology and evolution of cancer
%C Londres
%D 2017
%E Ujvari, B.
%E Roche, Benjamin
%E Thomas, F.
%L fdi:010072893
%G ENG
%I Elsevier Academic Press
%@ 978-0-12-804310-3
%P 219-222
%R 10.1016/B978-0-12-804310-3.00017-X
%U https://www.documentation.ird.fr/hor/fdi:010072893
%> https://www.documentation.ird.fr/intranet/publi/depot/2018-06-18/010072893.pdf
%W Horizon (IRD)
%X While it is widely acknowledged that intratumor heterogeneity is mostly generated by genomic instability, we propose that genomic instability is only part of a proximate mechanism that maintains intratumor heterogeneity through oncogenic selection. Within tissues and organs, malignant cells achieve greater success by cooperating in the process of tumor construction, rather than by just being in isolation. This process would involve the selection of a bet-hedging strategy during oncogenesis to generate the diversity of cell components needed to build, de novo, such an intricate cooperative system. This process requires sufficient time to generate the diversity of relevant clones, which may explain why solid tumors tend to occur late in life. In liquid environments, opportunities for structurally complex tumors are more limited. This may help explain why cancer cells from liquid tumors generally do not aggregate, are on average less heterogeneous (i.e., low selection for bet-hedging), and can be detrimental early in life (e.g., leukemia). In an evolutionary context, this suggests that the bet-hedging strategy is not only a universal risk-diversification strategy that evolves in the populations which face uncertain future and/or environment, it is also selected when there is a need of building, de novo, cooperative and complex systems.
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