Akademik Veri Yönetim Sistemi
Journal of Experimental and Clinical Medicine (Turkey), cilt.42, sa.1, ss.48-52, 2025 (Scopus)
Chronic myeloid leukemia (CML) is a myeloproliferative disease characterized by the BCR::ABL1 fusion gene. Despite the improved outcomes with the tyrosine kinase inhibitors (TKIs) treatment, primary and acquired resistance has become a big challenge. Through the various mechanisms, ABL1 tyrosine kinase domain (TKD) mutations play a major role in the resistance. Of the 287 patients in our study, 261 patients’ resistance status were available, and 110 (42.2%) were resistant to imatinib (IM). Ninety of those 110 patients’ BCR-ABL1 TKD mutation analyses were available, and 13 of them (14.4%) had mutations. 8 of them had the T315I mutation, 2 had the Y253H mutation, and the remaining patients had one E255K, V299L, and F317L mutation each. In the IM-resistant patients, the mean size of the spleen was larger, peripheral white blood cell count and plasma β2-microglobulin levels were higher, and hemoglobin and hematocrit levels were lower (p<0.05). Also, it could not be detected any significant correlation between fusion signal patterns and the rate of IM resistance. In conclusion, ABL1 TKD mutations are essential causes of TKI resistance in CML patients and must be used to choose the appropriate subsequent TKI.