Thomas Frédéric, DeGregori James, Marusyk Andriy, Dujon Antoine M, Ujvari Beata, Capp Jean-Pascal, Gatenby Robert, Nedelcu Aurora M
CREEC/CANECEV, MIVEGEC (CREES) Department, University of Montpellier, CNRS, IRD, Montpellier, France.
Department of Biochemistry and Molecular Genetics, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.
Evol Med Public Health. 2024 Sep 19;12(1):172-177. doi: 10.1093/emph/eoae021. eCollection 2024.
Tumorigenesis is commonly attributed to Darwinian processes involving natural selection among cells and groups of cells. However, progressing tumors are those that also achieve an appropriate group phenotypic composition (GPC). Yet, the selective processes acting on tumor GPCs are distinct from that associated with classical Darwinian evolution (i.e. natural selection based on differential reproductive success) as tumors are not genuine evolutionary individuals and do not exhibit heritable variation in fitness. This complex evolutionary scenario is analogous to the recently proposed concept of 'selection for function' invoked for the evolution of both living and non-living systems. Therefore, we argue that it is inaccurate to assert that Darwinian processes alone account for all the aspects characterizing tumorigenesis and cancer progression; rather, by producing the genetic and phenotypic diversity required for creating novel GPCs, these processes fuel the evolutionary success of tumors that is dependent on selection for function at the tumor level.
肿瘤发生通常归因于涉及细胞和细胞群之间自然选择的达尔文过程。然而，进展性肿瘤是那些也实现了适当的群体表型组成（GPC）的肿瘤。然而，作用于肿瘤GPC的选择过程不同于与经典达尔文进化相关的过程（即基于不同繁殖成功率的自然选择），因为肿瘤不是真正的进化个体，并且在适应性方面不表现出可遗传的变异。这种复杂的进化情况类似于最近提出的用于解释生物和非生物系统进化的“功能选择”概念。因此，我们认为断言仅达尔文过程就能解释肿瘤发生和癌症进展的所有特征是不准确的；相反，通过产生创造新GPC所需的遗传和表型多样性，这些过程推动了依赖于肿瘤水平功能选择的肿瘤的进化成功。
