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Understanding and overcoming resistance to tyrosine kinase inhibitors (TKIs) in Chronic myeloid leukemia (CML).
Expert Rev Hematol
January 2025
Hematology, Department of Translational and Precision Medicine, Sapienza University of Rome, Rome, Italy.
Introduction: Chronic myeloid leukemia (CML) represents one of the first neoplasms whose molecular pathogenesis was successfully unraveled, with tyrosine kinase inhibitors (TKIs) representing one of the first-targeted therapies. TKIs have revolutionized long-term outcomes of CML patients and their life expectancy. Nonetheless, a minority of patients will develop TKI resistance due to a complex and multifactorial process that ultimately leads to the emergence of an unresponsive cancer clone.
View Article and Find Full Text PDFThe acetylglucosaminyltransferase GnT-Ⅲ regulates erythroid differentiation through ERK/MAPK signaling.
J Biol Chem
December 2024
Division of Regulatory Glycobiology, Institute of Molecular Biomembrane and Glycobiology, Tohoku Medical and Pharmaceutical University, Sendai, Miyagi, Japan. Electronic address:
Differentiation therapy is an alternative strategy used in treating chronic myelogenous leukemia to induce the differentiation of immature or cancerous cells toward mature cells and inhibit tumor cell proliferation. We aimed to explore N-glycans' roles in erythroid differentiation using the sodium butyrate (NaBu)-induced model of K562 cells (WT/NaBu cells). Here, using lectin blot, flow cytometry, real-time PCR, and mass spectrometry analyses, we demonstrated that the mRNA levels of N-acetylglucosaminyltransferase Ⅲ ((encoded by the MGAT3 gene) and its product (bisected N-glycans) were significantly increased during erythroid differentiation.
View Article and Find Full Text PDFOlverembatinib After Failure of Tyrosine Kinase Inhibitors, Including Ponatinib or Asciminib: A Phase 1b Randomized Clinical Trial.
JAMA Oncol
January 2025
Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston.
Article Synopsis
Mebendazole effectively overcomes imatinib resistance by dual-targeting BCR/ABL oncoprotein and β-tubulin in chronic myeloid leukemia cells.
Korean J Physiol Pharmacol
January 2025
Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.
Article Synopsis
- Tyrosine kinase inhibitors (TKIs) are key treatments for chronic myeloid leukemia (CML), but resistance and intolerance to these drugs pose significant challenges.
- This research highlights the potential of re-purposed drug mebendazole (MBZ) as an effective anti-cancer agent that can work against both imatinib-sensitive and imatinib-resistant CML cells.
- MBZ was found to inhibit cell proliferation and induce cell death by targeting BCR/ABL activity, disrupting microtubule formation, and increasing DNA damage, presenting a novel approach for treating TKI-resistant CML patients.
Targeting splicing for hematological malignancies therapy.
BMC Genomics
November 2024
Department of Experimental Hematooncology, Medical University of Lublin, Chodzki 1, Lublin, 20-093, Poland.
Alterations in splicing patterns of leukemic cells have a functional impact and influence most cellular processes since aberrantly spliced isoforms can provide a proliferative advantage, enable to evade apoptosis, induce metabolic reprogramming, change cell signaling and antitumor immune response, or develop drug resistance. In this Review, we first characterize the general mechanism of mRNA processing regulation with a focus on the role of splicing factors, which are commonly mutated in blood neoplasms. Next, we provide a comprehensive summary on the current understanding of alternative splicing events, which confer resistance to targeted treatment strategies and immunotherapy.
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