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<p>Recurrent endometrial cancer has become a&#xa0;paradigm for biomarker-driven treatment in gynecologic oncology. Integration of The Cancer Genome Atlas Program (TCGA)-based classification into clinical practice, distinguishing DNA-polymerase&#xa0;ε (POLE)-mutated, mismatch repair-deficient/microsatellite instability-high (dMMR/MSI-H), no specific molecular profile (NSMP), and p53-abnormal tumors, has fundamentally changed risk stratification and treatment planning in the recurrent setting. While isolated locoregional recurrences may still be treated with curative intent, disseminated relapse requires individualized systemic strategies that account for tumor biology, prior therapy, and patient-related factors. Programmed cell death protein&#xa0;1 (PD-1) blockade is particularly effective in dMMR/MSI‑H disease, whereas endocrine strategies, lenvatinib plus pembrolizumab, and selected targeted approaches expand the therapeutic spectrum in mismatch repair-proficient (pMMR)/NSMP and p53-abnormal disease.</p>

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Therapie des Endometriumkarzinomrezidivs – molekulare Diagnostik als Wegweiser der personalisierten Behandlung

  • 期刊论文

  • 发表日期：

    2026年6月24日

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  • Marco J. Battista,
  • Eric Steiner

摘要

Recurrent endometrial cancer has become a paradigm for biomarker-driven treatment in gynecologic oncology. Integration of The Cancer Genome Atlas Program (TCGA)-based classification into clinical practice, distinguishing DNA-polymerase ε (POLE)-mutated, mismatch repair-deficient/microsatellite instability-high (dMMR/MSI-H), no specific molecular profile (NSMP), and p53-abnormal tumors, has fundamentally changed risk stratification and treatment planning in the recurrent setting. While isolated locoregional recurrences may still be treated with curative intent, disseminated relapse requires individualized systemic strategies that account for tumor biology, prior therapy, and patient-related factors. Programmed cell death protein 1 (PD-1) blockade is particularly effective in dMMR/MSI‑H disease, whereas endocrine strategies, lenvatinib plus pembrolizumab, and selected targeted approaches expand the therapeutic spectrum in mismatch repair-proficient (pMMR)/NSMP and p53-abnormal disease.