LAUSR

Since the introduction of imatinib ‘the first tyrosine kinase inhibitor (TKI)’ that targets BCR-ABL1, chronic myeloid leukemia (CML) has become a controlled malignancy at which patients with optimal responses would expect similar life expectancies of normal population [1]. Second-generation TKIs (2GTKIs; dasatinib, nilotinib, and bosutinib) and thirdgeneration TKI (ponatinib) were introduced as a salvage treatment option in patients with imatinib resistance or inadequate tolerability as well as a frontline alternative to imatinib [2,3]. Following a long-term TKI therapy, substantial portion of CML patients will achieve major molecular response (MMR); defined as a BCR-ABL1/ABL1 transcript ratio of ≤0.1%, also called MR [molecular response of three logs below an arbitrary standard baseline] expressed on international scale. A deep molecular response (DMR) is also defined as either MR (BCR-ABL1/ABL1 transcript ratio ≤0.01%) or MR (BCR-ABL1/ABL1 transcript ratio ≤0.0032%) [4]. Final update of the DASISION trial showed higher MR rates within 5 years among patients treated with dasatinib (43%) in comparison to imatinib-treated group (33%), determining the favorable outcomes of dasatinib as first-line treatment for CML [5]. Similarly, patients treated with nilotinib in ENESTnd trial had significant higher MR rates (300 mg twice daily, 54%; 400 mg twice daily, 52%) in comparison to imatinib group (31%) at 5 years of follow-up [6]. Although with a shorter follow-up period, BFORE trial indicated significantly higher rates of MR with bosutinib versus imatinib (8.1% vs. 3.3%) at 12 months [7].