Chronic Myeloid Leukemia (CML) is a hematological malignancy characterized by the presence of the BCR-ABL1 fusion gene, which leads to uncontrolled proliferation of leukemic cells. Despite the effectiveness of Tyrosine Kinase Inhibitors (TKIs) such as imatinib, dasatinib, and nilotinib in controlling CML, treatment resistance remains a major clinical challenge. The mechanisms contributing to resistance include BCR-ABL1 mutations, epigenetic modifications, and dysregulated microRNA (miRNA) expression. Gene expression profiling serves as a crucial tool for understanding disease progression, identifying novel therapeutic targets, and predicting treatment responses. This study explores the molecular basis of TKI resistance in CML through differential gene expression analysis, highlighting key biomarkers such as STAT5, BCL2L1 (Bcl-XL), MCL1, miR-150, and MYC. Additionally, we discuss emerging treatment strategies, including next-generation TKIs (asciminib, olverembatinib), non-BCR-ABL targeted therapies (mTOR inhibitors, JAK2 inhibitors, and HDAC inhibitors), and innovative approaches such as oncolytic viruses, exosome-based therapies, and CRISPR gene editing. Understanding the genetic and molecular landscape of CML can help optimize treatment strategies, improve early resistance detection, and advance personalized medicine for CML patients.
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Review Article |
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Infectious Diseases Received: 2025/10/11 | Accepted: 2025/12/12 | Published: 2025/12/30