Expression of genes potentially involved in loss of response in patients with chronic myeloid leukemia

• Published in: Gene 2024-02, Vol.896, p.148047-148047, Article 148047
• Main Authors: Benegas, Paula, Ziegler, Betiana, Dieminger, Victoria, Bengió, Raquel, Zapata, Pedro, Larripa, Irene, Ferri, Cristian
• Format: Article
• Language: English
• Subjects: Cell Proliferation; Drug Resistance, Neoplasm - genetics; Fusion Proteins, bcr-abl - genetics; Fusion Proteins, bcr-abl - metabolism; Humans; Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy; Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics; Protein Kinase Inhibitors - pharmacology
• ISSN: 0378-1119; 1879-0038
• DOI: 10.1016/j.gene.2023.148047

Chronic Myeloid Leukemia (CML) is a hematological malignancy characterized by the presence of the BCR::ABL1 fusion gene, which leads to uncontrolled cell growth and survival. Tyrosine kinase inhibitors (TKIs) have revolutionized the treatment of CML, but a significant proportion of patients develop resistance or lose response to these drugs. Understanding the molecular mechanisms underlying treatment response and resistance is crucial for improving patient outcomes. This study aimed to analyze the expression patterns of genes involved in treatment response and resistance in CML patients receiving TKI therapy. The expression levels of MET, FOXO3, p15, p16, HCK, and FYN genes were examined in CML patients and compared to healthy donors. Gene expression levels were compared between optimal responders (OR) and resistant patients (R) vs. healthy donors (HD). The MET and FOXO3 OR group showed significant differences compared with the HD, (p