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Author preprint presenting a theoretical model in which temporal–interstitial homeostasis functions as a distributed tissue-selection system influencing the competitive fitness of abnormal cell clones. The framework integrates circadian organization, microvascular exchange, interstitial transport, lymphatic flow, extracellular-matrix turnover, stromal activity, metabolism, innate immune surveillance, and tissue repair. It proposes testable mechanisms linking incomplete recovery and persistent repair-oriented tissue states to altered clonal selection in cancer.
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Kadir Gürel (2026) studied this question.
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