Abstract
Chronic myeloid leukemia (CML) is a clonal hematopoietic stem cell neoplasm characterized by the Philadelphia chromosome, t (9;22)(q34;q11.2), which causes the generation of the BCR-ABL1 oncoprotein with constitutively active tyrosine kinase. Treatment with tyrosine kinase inhibitors (TKIs) has significantly improved the prognosis of CML. Optimal treatment decisions at specific time points in patients with suboptimal response minimizes the risk of disease progression and CML-related death. The expected survival for patients with CML treated with TKI is now similar to that of the general population. Given the stable clinical course over the years, treatment-free remission (i.e., functional cure) can be considered in patients with sustained deep molecular response. Second-generation TKIs achieved higher rates of deep molecular response than imatinib, which could translate to increased candidates for functional cure without TKI therapy. The third-generation TKI, ponatinib, brought a new hope to patients who failed multiple TKIs because of resistance and/or intolerance. EUTOS long-term survival (ELTS) score can guide optimal treatment selection.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
