ArticleBritish journal of cancer2026
CDKN1B inactivation impacts ER signaling and drives resistance to endocrine therapy in breast cancer.
Article in British journal of cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundHormone receptor-positive (HR + ), HER2-negative breast cancer comprises ~70% of all breast cancer cases and is primarily treated with endocrine therapies such as tamoxifen, aromatase inhibitors, fulvestrant, and CDK4/6 inhibitors. However, resistance arises in ~40% of patients, limiting therapeutic efficacy.
methodWe performed integrated genomic, transcriptomic, and functional analyses of 186 HR + /HER2-tumors (88 sensitive, 98 resistant), to identify key drivers of endocrine hormone therapy resistance, Findings were validated functionally using in-vitro and in-vivo models.
resultsWe identify frequent CDKN1B (p27) loss-of-function mutations or deletions as a key and clinically actionable driver of endocrine resistance. CDKN1B knockdown in cell lines induces resistance to tamoxifen and fulvestrant, while its restoration re-sensitizes resistant cells. Importantly, CDKN1B-deficient tumors remain responsive to CDK4/6 inhibition, in vitro and in vivo. Immunohistochemistry and transcriptomic analysis of clinical cohorts (n = 138) and TCGA-METABRIC data (n = 1398) identify low p27 as an independent predictor of early relapse and poor survival.
conclusionOur results highlight CDKN1B as a prognostic biomarker to guide CDK4/6-targeted therapy and a predictor of endocrine resistance in HR + /HER2- breast cancer.
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