This work presents SCARBAC-T (Synthetic Cellular Agent for Redirection, Blockade and Collapse of Tumors), a conceptual framework that reinterprets cancer as a dynamic, communication-driven system. Rather than focusing solely on genetic mutations or tumor burden, the framework proposes that tumor resilience emerges from coordinated interactions between cancer stem cells, downstream populations, and the tumor microenvironment. SCARBAC-T introduces a Front–Spy–Jam–Flank architecture in which tumor state is inferred from dynamic biological signals, communication pathways are disrupted, and therapeutic interventions are applied in a coordinated, adaptive manner. The framework is explicitly positioned as a hypothesis-generating, non-clinical model. It does not propose a validated treatment protocol or clinical decision-making system, but instead outlines a systems-level approach intended to guide future computational, experimental, and translational research in adaptive oncology. By integrating concepts from tumor biology, adaptive therapy, and control theory, SCARBAC-T aims to contribute to emerging perspectives on closed-loop, patient-specific cancer treatment strategies.
Bert Jan van der Werf (Fri,) studied this question.