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Background <p>The tropomyosin receptor kinase (TRK) inhibitors have demonstrated substantial efficacy in solid tumors harboring neurotrophic tyrosine receptor kinase (NTRK) gene fusions. Although NTRK fusions have been sporadically reported in prostate cancer, their clinical significance and the therapeutic efficacy of TRK inhibitors in this disease remain unclear. We report a case of NTRK fusion-positive metastatic castration-resistant prostate cancer treated with the TRK inhibitor entrectinib.</p> Case presentation <p>A 68-year-old Japanese male with metastatic castration-resistant prostate cancer (mCRPC) experienced disease progression after androgen deprivation therapy, enzalutamide, abiraterone, and docetaxel. Because sufficient tumor tissue was unavailable for comprehensive genomic profiling, circulating cell-free DNA (cfDNA) analysis using FoundationOne<sup>®</sup> Liquid was performed, and a PBX1-NTRK1 fusion was identified. Based on this result, treatment with the TRK inhibitor, entrectinib, at a daily dose of 600&#xa0;mg was initiated. Despite two months of therapy, prostate-specific antigen levels increased from 22.7&#xa0;ng/mL to 70.2&#xa0;ng/mL, and bone scintigraphy demonstrated radiographic disease progression with new metastatic lesions. Although the patient reported transient improvement in bone pain, entrectinib was ultimately ineffective. No severe adverse events were observed.</p> Conclusion <p>To our knowledge, this is the first reported case of NTRK fusion-positive mCRPC treated with entrectinib. This case highlights the potential limitations of cfDNA-based detection of NTRK fusions in prostate cancer and suggests that NTRK fusions detected in cfDNA without tissue validation may not reliably predict clinical benefit from TRK inhibitors in mCRPC. Further studies are required to clarify the biological relevance of NTRK fusions and optimal patient selection for TRK inhibitors in prostate cancer.</p>

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NTRK fusion in metastatic castration-resistant prostate cancer treated with entrectinib: a case report

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月17日

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  • Shuichi Tatarano,
  • Akihiko Mitsuke,
  • Yoichi Osako,
  • Takashi Sakaguchi,
  • Satoru Inoguchi,
  • Ryosuke Matsushita,
  • Hirofumi Yoshino,
  • Yasutoshi Yamada,
  • Hideki Enokida

摘要

Background

The tropomyosin receptor kinase (TRK) inhibitors have demonstrated substantial efficacy in solid tumors harboring neurotrophic tyrosine receptor kinase (NTRK) gene fusions. Although NTRK fusions have been sporadically reported in prostate cancer, their clinical significance and the therapeutic efficacy of TRK inhibitors in this disease remain unclear. We report a case of NTRK fusion-positive metastatic castration-resistant prostate cancer treated with the TRK inhibitor entrectinib.

Case presentation

A 68-year-old Japanese male with metastatic castration-resistant prostate cancer (mCRPC) experienced disease progression after androgen deprivation therapy, enzalutamide, abiraterone, and docetaxel. Because sufficient tumor tissue was unavailable for comprehensive genomic profiling, circulating cell-free DNA (cfDNA) analysis using FoundationOne® Liquid was performed, and a PBX1-NTRK1 fusion was identified. Based on this result, treatment with the TRK inhibitor, entrectinib, at a daily dose of 600 mg was initiated. Despite two months of therapy, prostate-specific antigen levels increased from 22.7 ng/mL to 70.2 ng/mL, and bone scintigraphy demonstrated radiographic disease progression with new metastatic lesions. Although the patient reported transient improvement in bone pain, entrectinib was ultimately ineffective. No severe adverse events were observed.

Conclusion

To our knowledge, this is the first reported case of NTRK fusion-positive mCRPC treated with entrectinib. This case highlights the potential limitations of cfDNA-based detection of NTRK fusions in prostate cancer and suggests that NTRK fusions detected in cfDNA without tissue validation may not reliably predict clinical benefit from TRK inhibitors in mCRPC. Further studies are required to clarify the biological relevance of NTRK fusions and optimal patient selection for TRK inhibitors in prostate cancer.