632. Chronic Myeloid Leukemia: Therapy: Predictors of TKI Discontinuation and TFR Outcomes

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Conclusion cited from the abstract: These data indicate that as in adults, TKI may be safely discontinued also in children younger than 15 years of age at diagnosis, treated with TKI for ≥ 3 years, and sustained MR4.0 for ≥ 2 years, including patients who relapsed after HSCT. We suggest that plasma trough concentration level of imatinib may predict TFR for children with CML and sustained MR4.0 with imatinib. Further study of TKI discontinuation in children with CML is expected.

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Conclusion cited from the abstract: This retrospective study confirms the safety of TFR attempt and identifies variables strongly associated with prolonged TFR. The resulting predictive score presented here, if validated in larger patient cohorts, might help in tailoring the choice of TKI discontinuation to the individual patient. Also, most pts who lose MR4 inevitably lose MR3, suggesting the importance of a more intense monitoring strategy in this subgroup.

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Conclusion cited from the abstract: 

Based on a 15 years’ experience we were able to report on long term follow-up in TFR1 and in TFR2. Among patients experiencing molecular relapses, we observed 14% and 17% late relapses after more than 2 years after TFR1 and TFR2 respectively, suggesting that a long-term molecular follow-up is mandatory for CML patients in TFR.
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Conclusion cited from the abstract: 

This larger cohort confirms that TKIs could safely and successfully be discontinued a 2nd time in CP CML patients despite a 1st failure. The speed of molecular relapse after the 1st TKI discontinuation and TKI-free duration remain major factors significantly associated with TFR outcome.

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Figure: TFR according TKI-free duration after the 1st attempt of discontinuation

 

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Conclusion cited from the abstract: These results show that during a three year period, the D/C of Imatinib led to the increase of approximately 1 log in the tumour burden of non-relapsed pts, although none of them lost MMR and resumed treatment.
These data strongly indicate the need for a long-term monitoring of pts who D/C Imatinib; they also suggest that the functional status of residual CML cells rather than their number could represent the critical factor to predict the tumour load present after 3 years of Imatinib D/C.

 

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Conclusion cited from the abstract: 2G-TKI may be successfully stopped in CML pts with long-lasting MR4.5. Those without a history of suboptimal response or resistance have greatest chances of success. Sudden blast crisis is rare but unpredictable. Post-TKI discontinuation estimates of TFR change overtime. Together with that of molecular response type at specific time points, they represent important dynamic prognostic measures of outcome. They may also help individualizing molecular monitoring programs after TKI cessation.

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