Cancer as a Dysregulated Regenerative Response: A Functional Hypothesis on Systemic Signaling Collapse

This article introduces a new hypothesis regarding the systemic origin of cancer, framing it not as a random accumulation of malignant mutations but as a dysregulated continuation of an initially adaptive regenerative process. It proposes that chronic or unresolved tissue distress, whether inflammatory, metabolic, or biochemical, activates a repair program mediated by cytokines, immune signals, and growth factors. When internal feedback mechanisms, such as neuroendocrine, immune, or cellular signaling systems, fail to indicate completion, this regenerative response persists abnormally. The result is the emergence of a proliferative state that escapes systemic modulation. This model suggests that tumors are not pathological anomalies, but maladaptive extensions of biological repair efforts that have lost regulatory coherence. It opens a novel conceptual path for interpreting oncogenesis as a process of systemic miscommunication and calls for therapeutic strategies focused on signal recalibration and physiological reintegration, rather than exclusive cytotoxic eradication.