REVERSAL OF ACCELERATED PHASE CML WITH HIGH BLAST COUNT FOLLOWING 5+2 CHEMOTHERAPY AND DASATINIB: A CASE REPORT

Chronic Myeloid Leukemia (CML) typically progresses through chronic, accelerated, and blast phases, with most patients responding well to Tyrosine Kinase Inhibitors (TKIs) in the chronic phase. However, patients with Accelerated-Phase (AP) CML who develop high blast counts and TKI resistance are often considered at risk for transformation into Blast-Phase (BP) CML or secondary AML, requiring intensive chemotherapy or stem cell transplantation. This case highlights a patient with AP-CML who achieved full hematologic and molecular remission after receiving 5+2 chemotherapy and dasatinib, despite a high blast count and a prolonged TKI-free period before treatment initiation. A 44-year-old male was diagnosed with CML (February 2022) and initially treated with imatinib, followed by dasatinib, bosutinib, and nilotinib due to persistent BCR-ABL positivity and extreme thrombocytosis (> 1 million/µL). By October 2024, disease transformation was suspected due to BCR-ABL levels rising to 85% and bone marrow biopsy showing 17% blasts. Notably, the patient had discontinued dasatinib at least three months before hospitalization, further contributing to disease progression. Given the high blast count and persistent thrombocytosis, 5+2 induction chemotherapy (cytarabine + idarubicin) was administered, followed by a reassessment bone marrow biopsy in December 2024, which was inconclusive. Post-chemotherapy, the patient refused further AML-directed treatment and instead resumed dasatinib therapy. Over the following six months, the patient’s hematologic parameters normalized, and repeat bone marrow biopsy confirmed complete remission, demonstrating a remarkable reversal from the accelerated phase. This case illustrates the potential for AP-CML with a high blast count to revert to the chronic phase following 5+2 chemotherapy and re-initiation of TKI therapy. It also underscores the risks associated with TKI discontinuation in advanced CML and suggests that targeted therapy with TKIs can remain effective even after transient chemotherapy-induced cytoreduction. This highlights the importance of individualized treatment approaches in advanced CML and the potential for avoiding AML-directed therapies in select cases.