ReviewJournal of the Egyptian National Cancer Institute2025
Current and future of targeted therapies against BCR::ABL kinases.
Review in Journal of the Egyptian National Cancer Institute, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed.
- Pharmaceutical Compounding as a Pillar of Personalized Oncology: Current Applications, Emerging Technologies, and Future Perspectives.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Rational Design, Synthesis, and Molecular Docking of Novel Terpene Analogues of Imatinib, and Their Inhibition on Downstream BCR-ABL Signaling.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Bone Marrow Edema and Tyrosine Kinase Inhibitors Treatment in Chronic Myeloid Leukemia.Diagnostics (Basel, Switzerland) · 2025Article
- Reversine-Induced Telomere Architecture Remodeling in Chronic Myeloid Leukemia Cell Lines: Insights from TeloViewCurrent issues in molecular biology · 2025Article
- Natural Products Targeting BCR-ABL: A Plant-Based Approach to Chronic Myeloid Leukemia Treatment.Molecules (Basel, Switzerland) · 2025Review
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic myeloid leukemia (CML) is a kind of leukemia that arises due to the translocation betwixt chromosomes 9 and 22. Philadelphia chromosome is characterized by the BCR::ABL fusion gene, which results from this recombination. It transcribes into active tyrosine kinase variants such as P185, P190, P210, and P230, depending on breakpoint chain variations. The fusion protein, encodes tyrosine kinases with varying exons, resulting in uncontrollable ATP-utilizing downstream signaling activities. Targeted therapy with various tyrosine kinase inhibitors (TKIs) is used to combat BCR::ABL fusion kinases and increase the survival rate of patients. However, the incidence of TKI resistance among CML patients is widely noticed around the world. Hence, an elaborate and accurate understanding of the structural interactions between BCR::ABL encoded tyrosine kinases, which are responsible for sensitivity and resistance, is mandatory for hassle-free targeted therapy. This review is intended to cover the reported structural interactions between BCR::ABL variants and TKI ligands in detail to highlight strategies that may be applied in the near future to overcome the resistance and other cross-reactions.
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Registered trials
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