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<p>Triple-negative apocrine carcinoma (TNAC) is a rare and chemotherapy-insensitive subtype of triple-negative breast cancer (TNBC), characterized by specific morphology and molecular features. Despite limited chemotherapy response, TNAC shows favorable long-term survival, suggesting distinct resistance mechanisms. In this study, we present the first proteomics-based profiling of TNAC formalin-fixed paraffin-embedded (FFPE) samples using mass spectrometry. Our analysis reveals progressive activation of PI3K/AKT and androgen receptor (AR) signaling, along with upregulation of GTPase-related proteins, suggesting enhanced invasiveness. Post-chemotherapy TNAC displays increased inflammation and mixed ribosomal regulation, pointing to a metabolic shift in survival strategy. These findings support the rationale for exploring chemotherapy de-escalation strategies in TNAC, and highlight the potential utility of PI3K/AKT inhibitors and AR antagonists, possibly in combination with GTPase inhibitors, metabolic disruptors, or immunotherapy.</p>

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Proteomics characterization of triple-negative apocrine carcinoma reveals molecular features of progression and chemotherapy response

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月13日

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  • Yiying Zhu,
  • Mengping Long,
  • Wenhao Shi,
  • Tianlong He,
  • Fangzhou Xie,
  • Annan Qian,
  • Yuqiao Liu,
  • Taobo Hu,
  • Shaojun Tang

摘要

Triple-negative apocrine carcinoma (TNAC) is a rare and chemotherapy-insensitive subtype of triple-negative breast cancer (TNBC), characterized by specific morphology and molecular features. Despite limited chemotherapy response, TNAC shows favorable long-term survival, suggesting distinct resistance mechanisms. In this study, we present the first proteomics-based profiling of TNAC formalin-fixed paraffin-embedded (FFPE) samples using mass spectrometry. Our analysis reveals progressive activation of PI3K/AKT and androgen receptor (AR) signaling, along with upregulation of GTPase-related proteins, suggesting enhanced invasiveness. Post-chemotherapy TNAC displays increased inflammation and mixed ribosomal regulation, pointing to a metabolic shift in survival strategy. These findings support the rationale for exploring chemotherapy de-escalation strategies in TNAC, and highlight the potential utility of PI3K/AKT inhibitors and AR antagonists, possibly in combination with GTPase inhibitors, metabolic disruptors, or immunotherapy.