Changes to This Summary (01/27/2015)
The PDQ cancer information summaries are reviewed regularly and updated as new information becomes available. This section describes the latest changes made to this summary as of the date above.
Updated statistics with estimated new cases and deaths for 2015 (cited American Cancer Society as reference 1).
Added text to state that in randomized prospective trials, nilotinib and dasatinib show higher rates of earlier molecular response compared with imatinib; whether this will translate to improved long-term outcomes is unclear (cited Hughes et al. as reference 10 and Jabbour et al. as reference 11 and level of evidence 1iiDiv).
Added text to state that a BCR/ABL transcript level of less than 10% in patients after 3 months of treatment with a specific tyrosine kinase inhibitor is associated with the best prognosis in terms of failure-free survival, progression-free survival (PFS), and overall survival (cited Marin et al. [Journal of Clinical Oncology 2012] as reference 13, 2012 Branford et al. as reference 14, Marin et al. [Blood 2012] as reference 15, and Neelakantan et al. as reference 16). Also added that in a retrospective analysis, even patients with a BCR/ABL transcript level greater than 10% after 3 months of therapy did well when the halving time was less than 76 days; however, mandating a change of therapy based on this 10% transcript level at 3 to 6 months is problematic because 75% of patients do well even with a suboptimal response (cited 2014 Branford et al. as reference 17 and Baccarani et al. as reference 18).
Added Hehlmann et al. as reference 23.
Added text to state that the investigators in the According to Stop Imatinib study have shown that molecular remission can be re-established anecdotally after restarting therapy (cited Rousselot et al. as reference 29).
Revised text to state that in particular, the T315I mutation marks resistance to imatinib, dasatinib, nilotinib, and bosutinib; a phase II study with 449 patients, indicated that 60% of the 129 patients with the T315I mutation had a molecular response to ponatinib, an oral tyrosine kinase inhibitor (cited Cortes et al. as reference 20 and level of evidence 3iiiDiv). Also added that ponatinib has activity in heavily pretreated-resistant CML and in a third of the patients with accelerated-phase or blast-crisis phase CML.
This summary is written and maintained by the PDQ Adult Treatment Editorial Board, which is editorially independent of NCI. The summary reflects an independent review of the literature and does not represent a policy statement of NCI or NIH. More information about summary policies and the role of the PDQ Editorial Boards in maintaining the PDQ summaries can be found on the About This PDQ Summary and PDQ NCI's Comprehensive Cancer Database pages.