Initial therapy with ponatinib in patients with chronic-phase CML yields high cytogenetic and molecular responses early in treatment but dose reductions due to toxicity were common.
A nonsignificant trend was seen toward higher MMR rates with nilotinib vs imatinib in patients with a suboptimal response after 18-24 months of initial imatinib treatment.
Reduction of BCR-ABL transcripts to 0.35 fold of baseline within 3 months on imatinib better predicted 5-year PFS and OS than 3-month BCR-ABLIS < 10%.
BCR-ABL level reduction between 3 and 6 months on TKI therapy increased OS, PFS, and failure-free survival and achievement of major molecular response.
Highly sensitive ultradeep sequencing–based screening identifies low-level TKI resistance mutations that can better inform second- or third-line therapy decisions.
Patients show early and durable cytogenetic and hematologic responses as well as high rates of hypertension and increasing vascular occlusive events with longer treatment duration in the 2-year follow-up of the PACE trial.
Dasatinib-treated patients show deeper molecular responses and fewer disease transformations compared with imatinib.
Nilotinib shows increased rate of early molecular responses, which translates to improved survival and higher rates of MR4.5 at the 5-year follow-up.
Dasatinib was associated with higher rates of molecular response than imatinib, but also higher rates of missed doses and treatment reductions.
Although the primary endpoint of improved CCyR rate was not met, analyses of secondary endpoints accounting for treatment crossover suggest that switching to nilotinib may be associated with higher cytogenetic and molecular response rates than imatinib dose escalation.
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