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To investigate the role of MCM2 and the origin licensing complex in resistance to CDK4/6 inhibitors and endocrine therapy in breast cancer.

MCM2 and Origin Licensing Complex in ER+/HER2- Breast Cancer Therapy Resistance

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To investigate the role of MCM2 and the origin licensing complex in resistance to CDK4/6 inhibitors and endocrine therapy in breast cancer.
Conducted a retrospective analysis on treatment-naive ER+/HER2- breast cancer cohort with 1,960 patients.
Performed NGS profiling on biopsies to analyze gene expression and mutations.
Stratified tumors by MCM2 and LC gene set expression levels into high and low groups.
Employed statistical tests like chi-square and Fisher’s Exact to analyze molecular variables.
MCM2-high tumors showed a dominant LumB subtype compared to MCM2-low tumors (85.5% vs 39.8%).
MCM2-high tumors exhibited enrichment in pathways related to PI3K/AKT/mTOR and E2F/MYC.
Higher frequency of TP53 mutations in MCM2-high tumors compared to low (32.6% vs 16.6%).
Notable gene expression correlation between MCM2 and MKI67 (Spearman’s ρ=0.77).

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Retrospective review identifies MCM2 as a potential biomarker for resistance in ER+/HER2- breast cancer, suggesting new treatment strategies.

Raghavan et al. (2026) studied this question.

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Retrospective review identifies MCM2 as a potential biomarker for resistance in ER+/HER2- breast cancer, suggesting new treatment strategies.