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October 12, 2025Open Access

Overexpression of Proteins Involved in Mitotic Progression Underlies High Proliferation and Chromosomal Instability in Androgen Receptor-Low Triple-Negative Breast Cancer

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Authors

PRPadmashree C.G. RidaRARaphael AndreaeNBNoah Bikhazi

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Overview

This review reveals how high proliferation and chromosomal instability manifest in AR-low TNBC, suggesting key molecular targets for therapy.

Key Points

  • AR-low TNBC shows rapid proliferation alongside chromosomal instability, which drives tumor evolution and treatment resistance.
  • The research highlights a FoxM1–WDR5–ASPM axis that promotes mitotic dysregulation, enhancing tumor growth and intra-tumoral diversity.
  • TP53 mutations exacerbate the dysregulated network, allowing aneuploid cells to survive, thus impacting cancer progression and treatment response.
  • Understanding these pathways may reveal actionable therapeutic strategies to combat high proliferation in genomically unstable cancers.

Cite This Study

Rida et al. (2025) studied this question.

synapsesocial.com/papers/68ebc91af2c3e4d8d926e33fhttps://doi.org/10.20944/preprints202510.0602.v1
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1FOXM1 Signaling Network Transcriptionally Upregulates Expression of Proteins Involved in Mitotic Progression to Induce High Proliferation and Chromosomal Instability in Androgen Receptor-Low Triple-Negative Breast Cancer2026
  2. 2Integrative proteogenomics and forward genetics reveals a novel mitotic vulnerability in triple-negative breast cancer.2025
  3. 3Constitutive androgen receptor activity sustains DNA replication programs in triple-negative breast cancer2026
  4. 4NFYA-Mediated TTK Up-Regulation Drives Fast Cell Cycle Progression and Its Inhibition Leads to Mitotic Catastrophe in Triple Negative Breast Cancer2026
  5. 5Mitotic kinases are emerging therapeutic targets against metastatic breast cancer2024 · 7 citations