What does this research mean for the field?

Post-transplant tyrosine kinase inhibitor (TKI) therapy significantly improves 3- and 5-year overall survival in chronic myeloid leukemia patients undergoing allogeneic hematopoietic stem cell transplantation, despite an association with higher rates of chronic graft-versus-host disease. Novelty: ClaimNovelty.CONFIRMATORY. Consensus alignment: ConsensusAlignment.SUPPORTS_CONSENSUS.

What question did this study set out to answer?

This research aims to assess the impact of post-transplant tyrosine kinase inhibitor therapy on long-term survival and graft-versus-host disease outcomes in patients with chronic myeloid leukemia.

May 30, 2026

Survival impact of post-transplant tyrosine kinase inhibitor therapy in chronic myeloid leukemia.

Key Points

This research aims to assess the impact of post-transplant tyrosine kinase inhibitor therapy on long-term survival and graft-versus-host disease outcomes in patients with chronic myeloid leukemia.
Identified adult CML patients undergoing allo-HSCT between January 2010 and June 2025.
Cohorts categorized by TKI exposure within 3 months post-transplant and matched 1:1 using propensity scores.
Survival and GVHD outcomes evaluated using Kaplan–Meier and Cox regression analyses.
At 3 years, OS was 72.67% for TKI vs 58.90% for no TKI (HR 0.57, 95% CI 0.389–0.837, p=0.0036).
At 5 years, OS was 68.75% for TKI vs 55.31% for no TKI (HR 0.588, 95% CI 0.407–0.851, p=0.0043).
Chronic GVHD rates were higher among TKI-treated patients (37.14% vs 24.57%, OR 1.81, 95% CI 1.14–2.88, p=0.011).

Abstract

e18599 Background: Although tyrosine kinase inhibitors (TKIs) have reduced the need for allogeneic hematopoietic stem cell transplantation (allo-HSCT) in chronic myeloid leukemia (CML), transplantation remains necessary for patients with TKI resistance, intolerance, or disease progression. Post-transplant TKI maintenance is widely used, yet real-world data evaluating its impact on overall survival (OS) and graft-versus-host disease (GVHD) are limited. We assessed the association between post-HSCT TKI use and long-term survival and GVHD outcomes. Methods: Adult CML patients undergoing allo-HSCT between January 2010 and June 2025 were identified in the TriNetX Research Network and categorized by TKI exposure within 3 months post-transplant. Cohorts were propensity score matched 1:1. OS was evaluated using Kaplan–Meier and Cox regression for 3 and 5 years. A landmark analysis beginning on day 30 was performed to address immortal time bias. Secondary outcomes included chronic GVHD within 1 year. Results: After matching, 350 patients were included (175 TKI vs 175 no TKI). At 3 years from transplant (day 0), OS was significantly higher with TKI therapy (72.67% vs 58.90%; HR 0.57, 95% CI 0.389–0.837; log-rank p=0.0036), with consistent landmark results (73.51% vs 59.93%; HR 0.566, 95% CI 0.383–0.838; p=0.0040). At 5 years, OS remained superior (68.75% vs 55.31%; HR 0.588, 95% CI 0.407–0.851; p=0.0043), with similar landmark findings (69.55% vs 56.27%; HR 0.585, 95% CI 0.402–0.853; p=0.0048). Chronic GVHD within 1 year was more frequent among TKI-treated patients (37.14% vs 24.57%; OR 1.81, 95% CI 1.14–2.88; p=0.011). Conclusions: Post-transplant TKI therapy was associated with significantly improved 3- and 5-year OS in patients with CML undergoing allo-HSCT, including landmark analysis. Higher rates of chronic GVHD may reflect confounding by indication and longer survival rather than a direct causal effect. These findings support post-HSCT TKI maintenance as an important survival-enhancing strategy in CML.

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