Oncogenic signaling drives cells into states of elevated demand, requiring sustained biosynthesis, coordinated intracellular trafficking, precise mitotic execution, and ongoing coupling to the tumor microenvironment.
As demand rises, redundancy narrows and the cellular architecture becomes dependent on a limited set of structural functions that maintain cell-wide organization, rather than merely sustaining local pathway activity. In advanced malignant states, persistence reflects feasibility within narrow architectural limits, rather than robustness or adaptability in the conventional sense.
