Introduktion. The introduction of tyrosine kinase inhibitors (TKIs) has radically changed the prognosis for patients with chronic myeloid leukemia (CML): the median survival with targeted therapy is estimated at 25–30 years [1]. TKIs have made it possible to observe the disease course over longer periods. One of the unresolved issues is the development of a new myeloproliferative disorder on the background of an existing one. The causes and management strategies for patients who develop parallel myeloproliferative neoplasms represent an emerging area for further research.

Aim. To describe a clinical case of chronic myelomonocytic leukemia (CMML) arising in a patient with CML during treatment with TKIs.

Materials and methods. Clinical and laboratory data of the patient collected between 2016 and 2025 were analyzed, including complete blood count, myelogram, immunophenotyping, cytogenetic, and molecular genetic studies. In addition, the clinical course of the disease and response to TKI therapy were assessed. A literature search was conducted in Google Scholar and NCBI databases using specific keywords to identify comparable clinical cases.

Results. We describe a clinical case of a 53-year-old patient with CML who, after long-term TKI therapy (imatinib for 5 years, nilotinib for 2 years) and achievement of a deep molecular response, developed CMML, followed six months later by transformation into acute myeloid leukemia (AML). The nature of this phenomenon remains unclear. A possible mechanism may involve the emergence of a new independent clone after eradication of CML clones under TKI therapy. Another explanation may be mutational transformation of the CML clone due to the effect of TKIs or other factors. Comprehensive molecular genetic testing at the stage of initial diagnosis is important for monitoring potential clonal evolution and transformation of myeloproliferative neoplasms within a single origin.

Conclusions. Clinical scenarios in patients undergoing long-term TKI therapy remain insufficiently studied. Such patients require regular monitoring, with particular attention to the possible emergence of new clones or CML transformation. Currently, the number of reported cases of concomitant CML and CMML remains limited, likely due to the relatively recent introduction of TKIs into clinical practice. This may represent only an initial stage of data accumulation, while further observations will help clarify the mechanisms of parallel clonal processes and optimize management strategies.

Keywords: chronic myeloid leukemia, CML, BCR::ABL1, tyrosine kinase inhibitors (TKIs), imatinib, nilotinib, chronic myelomonocytic leukemia, CMML.