Cancer as an Informational Attractor Transition. A Prigoginian Informational Dissipation (PID) Hypothesis

Cancer has historically been interpreted predominantly through the somatic mutation theory, which emphasizes mutation accumulation, clonal selection, and evolutionary adaptation. However, this mutation-centered interpretation is increasingly being reconsidered in light of alternative frameworks emphasizing tissue organization, epigenetic regulation, metabolic dysfunction, and systems-level processes. Although genetic alterations remain central to many cancers, they may not provide a sufficient or universally applicable explanation for malignant transformation. These developments highlight the need for complementary theoretical approaches capable of integrating molecular mechanisms with the emergence and persistence of malignant phenotypes. Here, a complementary theoretical framework based on Prigoginian Informational Dissipation (PID) is proposed. In this model, multicellular organisms are viewed as hierarchical dissipative structures that maintain low informational entropy through coordinated information processing. Healthy cellular subsystems are embedded within a global organismal attractor characterized by memory, relatedness, and end-oriented informational dissipation. Alterations in regulatory organization, cellular memory, and multicellular constraints may weaken informational relatedness, allowing a cellular subsystem to become progressively uncoupled from the organismal attractor. Such a transition need not depend on accumulated molecular damage and may also involve the increased expression of evolutionarily conserved cellular functions normally constrained by multicellular organization. Following loss of multicellular regulatory integration, autonomous proliferation may further disrupt organism-level informational organization, generating hypothesized positive feedback between clone expansion and informational disintegration. The hypothesis is explored using reduced phenomenological dynamical equations, including an explicit entropy-proliferation coupling. The reduced clone model exhibits conditions for bistability, while the broader implications for immune recognition, aging, tumour dormancy, and cancer evolution remain theoretical and require further mathematical and experimental validation. The framework therefore proposes testable relationships between informational integration and malignant persistence rather than a completed quantitative theory of carcinogenesis.