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<p>Triple-negative breast cancer (TNBC) has become a clinical challenge due to its high invasiveness, the lack of clear therapeutic targets, and the limitations of existing treatment methods. It is worth noting that although TNBC is the subtype with the highest immune infiltration and the best response to immune checkpoint inhibitor (ICI), the response rate of ICI monotherapy for TNBC is only 15-20%, which could be partially explained by its “cold tumor” characteristics, not allowing an adequate immune response activation to be primed. Although the pathological complete response rate (pCR) of ICI combined with chemotherapy in trials such as Keynote 522 exceeded 50%. However, the core characteristics of “cold tumors”—including insufficient immune cell infiltration (such as cytotoxic T lymphocyte (CTL) deficiency) and a strong immunosuppressive microenvironment—remain key factors affecting further improvement of therapeutic efficacy. Therefore, transforming “cold tumors” into “hot tumors” (i.e., immune inflammatory tumors) is a key scientific issue for enhancing the efficacy of TNBC immunotherapy.</p>

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The “Cold Tumor” to “Hot Tumor” transformation strategy for triple-negative breast cancer: from mechanism to clinical translation

  • 期刊论文

  • 发表日期：

    2026年1月2日

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  • Hong Wang,
  • Feilong Li,
  • Pandeng Hao,
  • Yongliang Mei

摘要

Triple-negative breast cancer (TNBC) has become a clinical challenge due to its high invasiveness, the lack of clear therapeutic targets, and the limitations of existing treatment methods. It is worth noting that although TNBC is the subtype with the highest immune infiltration and the best response to immune checkpoint inhibitor (ICI), the response rate of ICI monotherapy for TNBC is only 15-20%, which could be partially explained by its “cold tumor” characteristics, not allowing an adequate immune response activation to be primed. Although the pathological complete response rate (pCR) of ICI combined with chemotherapy in trials such as Keynote 522 exceeded 50%. However, the core characteristics of “cold tumors”—including insufficient immune cell infiltration (such as cytotoxic T lymphocyte (CTL) deficiency) and a strong immunosuppressive microenvironment—remain key factors affecting further improvement of therapeutic efficacy. Therefore, transforming “cold tumors” into “hot tumors” (i.e., immune inflammatory tumors) is a key scientific issue for enhancing the efficacy of TNBC immunotherapy.