This manuscript presents a systems-level oncology framework examining how chronic CB1-dominant signalling may influence immune surveillance dynamics over extended timescales. Rather than proposing direct carcinogenic action, the paper advances a coordination-based model in which adaptive immune timing, expansion depth, and microenvironmental regulation gradually recalibrate under sustained modulation. The analysis integrates innate–adaptive immune transitions, T cell proliferation and effector persistence, cytokine waveform alignment, regulatory phenotype balance, and tumour microenvironment stabilisation. Particular attention is given to checkpoint-dependent antitumour immunity and the conditions under which partial modulation of activation thresholds may alter elimination probability. The framework proposes that tumour permissivity can emerge from incremental reductions in immune coordination rather than overt suppression. These shifts are context-dependent and influenced by biological reserve, age, metabolic state, and therapeutic environment. This paper forms part of the Series 2 expansion of the Context-Dependent THC framework, which examines long-term adaptive system modulation across metabolic, autonomic, endocrine, and immune domains. The model is hypothesis-generating, explicitly probabilistic, and structured to support future longitudinal empirical testing.
Anwar Mohamed (Thu,) studied this question.