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Life sciences · Journal article
PLOS One · November 5, 2026
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In this retrospective public-cohort observational study, we evaluated a biologically motivated extracellular matrix (ECM)-high/immune-low transcriptomic score for association with pathological complete response (pCR) after neoadjuvant therapy in breast cancer. The score contrasted standardized ECM/fibroblast and immune-response components. Cohort-specific logistic models adjusted for available clinical covariates; their performance was evaluated separately and was not validation of a locked transported model. In I-SPY2/GSE194040 (n = 987; 319 pCR events), a one-standard-deviation higher score was associated with lower pCR odds (odds ratio [OR] 0.687, 95% confidence interval [CI] 0.588–0.803). Inverse adjusted estimates were also observed in GSE25066 (OR 0.744, 95% CI 0.568–0.975) and GSE20271 (OR 0.407, 95% CI 0.232–0.715). Apparent areas under the receiver operating characteristic curve (AUCs) for these multivariable models were 0.750, 0.732 and 0.798; corresponding 500-bootstrap optimism-corrected estimates were 0.731, 0.713 and 0.765, conditional on processed scores. GSE20194 estimates were nonsignificant, and substantial record overlap with GSE25066 prevented interpretation as additional independent confirmation. A GSE25066 sensitivity restricted to deposited human epidermal growth factor receptor 2 (HER2)-negative status retained direction but had a confidence interval crossing unity. Higher scores correlated with lower immune-related reverse-phase protein array signals in matched I-SPY2 samples. The findings support a hypothesis-generating bulk-transcriptomic response association, with limited cross-cohort robustness. Heterogeneous treatment, sampling, assay and endpoint annotations, together with absent spatial and prospective validation, preclude claims of causality or clinical treatment-selection utility.