<p>Achieving treatment-free remission (TFR) in patients with chronic myeloid leukemia (CML) requires several years of tyrosine kinase inhibitor (TKI) therapy and a sustained deep molecular response (DMR). We report an exceptional case of a 54-year-old woman who achieved long-term TFR despite discontinuing dasatinib after only 9&#xa0;months due to grade 3 interstitial pneumonitis. At the time of discontinuation, the duration of DMR was 128&#xa0;days. Following cessation, BCR::ABL1 transcript levels transiently rebounded to 0.0729% on the International Scale but subsequently declined spontaneously without resumption of TKI therapy. The patient has remained in TFR for more than 7&#xa0;years. Immunological analysis revealed clonal expansion of a unique CD56<sup>+</sup>CD57<sup>+</sup>CD8<sup>dim</sup> T-cell population possessing natural killer (NK)-like properties, as confirmed by T-cell receptor gene rearrangement analysis. This specific clone persisted after discontinuation, suggesting a role in the sustained immune surveillance of residual leukemia stem cells. These findings suggest that the quality of immune reconstitution, specifically the induction of innate-like effector T-cell clones, may be a more critical determinant of TFR success than the absolute duration of therapy.</p>

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Long-term treatment-free remission in CML after early dasatinib discontinuation due to interstitial pneumonitis

  • Makoto Kashimura,
  • Yuki Fujioka,
  • Yong-Mei Guo,
  • Teruko Takahashi,
  • Keiichi Moriya,
  • Naoto Takahashi

摘要

Achieving treatment-free remission (TFR) in patients with chronic myeloid leukemia (CML) requires several years of tyrosine kinase inhibitor (TKI) therapy and a sustained deep molecular response (DMR). We report an exceptional case of a 54-year-old woman who achieved long-term TFR despite discontinuing dasatinib after only 9 months due to grade 3 interstitial pneumonitis. At the time of discontinuation, the duration of DMR was 128 days. Following cessation, BCR::ABL1 transcript levels transiently rebounded to 0.0729% on the International Scale but subsequently declined spontaneously without resumption of TKI therapy. The patient has remained in TFR for more than 7 years. Immunological analysis revealed clonal expansion of a unique CD56+CD57+CD8dim T-cell population possessing natural killer (NK)-like properties, as confirmed by T-cell receptor gene rearrangement analysis. This specific clone persisted after discontinuation, suggesting a role in the sustained immune surveillance of residual leukemia stem cells. These findings suggest that the quality of immune reconstitution, specifically the induction of innate-like effector T-cell clones, may be a more critical determinant of TFR success than the absolute duration of therapy.