Living systems exist exclusively as open systems far from thermodynamic equilibrium. The distinction between healthy tissue and oncogenic processes does not lie in the magnitude of non-equilibrium, but in the manner of its regulation. This conceptual hypothesis proposes that the physical state of the cellular membrane constitutes a primary regulatory element that determines whether energetic and material fluxes are bound into a stable, hierarchically regulated organization or diverted into a primitive, deregulated regime characteristic of tumor growth. In healthy tissue, membrane properties such as optimal fluidity, selective permeability, and stable lateral microdomains enable controlled energy dissipation and efficient entropy export, sustaining long-term dynamic stability. In contrast, oncogenic processes are associated with altered membrane states marked by increased fluidity, loss of microdomain organization, and reduced selectivity, leading to unbound fluxes, elevated local entropy production, and progressive destabilization of the tissue environment. Within this framework, cancer is interpreted not as a return to equilibrium or solely a genetic failure, but as the collapse of regulated non-equilibrium at the membrane level, with genetic alterations emerging as secondary adaptations.
Peter Mikuláš (Mon,) studied this question.