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<p>Hormone receptor (HR)-positive is the most common subtype in female breast cancer (BC) patients, and endocrine therapy (ET) is the primary treatment for HR-positive BC. Clinical studies have confirmed that cyclin-dependent kinase 4/6 (CDK4/6) inhibitors combined with ET can significantly prolong the progression-free survival (PFS) of advanced BC patients. Consequently, the combination of CDK4/6 inhibitors and ET has been established as a first-line treatment for advanced HR-positive BC or a standard treatment following ET progression. However, the regimen after CDK4/6 inhibitor treatment failure remains highly controversial, and the reported clinical outcomes of CDK4/6 inhibitor rechallenge are inconsistent. Preclinical studies have collected evidence suggesting that multiple mechanisms may contribute to intrinsic or acquired resistance to CDK4/6 inhibitors. Future research should further investigate the translational relationship between resistance mechanisms and clinical efficacy, and identify biomarkers to screen the benefit population from CDK4/6 inhibitor rechallenge therapy, developping individualized treatment strategies.</p>

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CDK4/6 inhibitor rechallenge therapy in advanced breast cancer

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年12月20日

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  • Yuhan Sun,
  • Yang Zhao,
  • Xinyang Yu,
  • Yuanfu Qi,
  • Xin Dai

摘要

Hormone receptor (HR)-positive is the most common subtype in female breast cancer (BC) patients, and endocrine therapy (ET) is the primary treatment for HR-positive BC. Clinical studies have confirmed that cyclin-dependent kinase 4/6 (CDK4/6) inhibitors combined with ET can significantly prolong the progression-free survival (PFS) of advanced BC patients. Consequently, the combination of CDK4/6 inhibitors and ET has been established as a first-line treatment for advanced HR-positive BC or a standard treatment following ET progression. However, the regimen after CDK4/6 inhibitor treatment failure remains highly controversial, and the reported clinical outcomes of CDK4/6 inhibitor rechallenge are inconsistent. Preclinical studies have collected evidence suggesting that multiple mechanisms may contribute to intrinsic or acquired resistance to CDK4/6 inhibitors. Future research should further investigate the translational relationship between resistance mechanisms and clinical efficacy, and identify biomarkers to screen the benefit population from CDK4/6 inhibitor rechallenge therapy, developping individualized treatment strategies.