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Life sciences · Journal article
Frontiers in Oncology · October 12, 2026
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Treatment resistance is usually attributed to genetic or adaptive changes within tumor cells. Here, we propose that, in some tumors, resistance also depends on specific interactions between malignant and non-malignant cells. We define relational resistance as a resistant phenotype that requires the functional organization of particular intercellular relationships. This concept is narrower than microenvironment-mediated resistance: the presence of stromal, immune, or vascular cells is not sufficient to establish relational resistance; a defined interaction must contribute functionally to treatment failure. We organize evidence along a five-step sequence: predicted edge, spatial support, functional edge, relational dependency, and therapeutic vulnerability. Genitourinary cancers illustrate different positions along this sequence: bladder cancer provides a predicted CD6–ALCAM edge with independent clinical association but without targeted perturbation; prostate cancer provides myeloid circuits with preclinical causal support and phase 1 proof-of-concept targetability; and renal cell carcinoma provides spatially organized multicellular programs with functional and preclinical perturbation support. We further propose relational memory as the hypothesis that a treatment-induced or treatment-selected interaction persists after therapy and influences response to a subsequent treatment. The framework therefore shifts the therapeutic question from which resistant cells are present to which relationships are required for resistance to persist.