ReviewHandbook of experimental pharmacology2023
Molecular Mechanisms of Tyrosine Kinase Inhibitor Resistance in Chronic Myeloid Leukemia.
Review in Handbook of experimental pharmacology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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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
8 citing papers in PubMed, 8 citations in OpenAlex.
- A combination of artemisinin, moxidectin, and doxorubicin drugs can selectively and efficiently induce apoptosis in acute lymphoblastic and chronic myeloid leukemia cells in vitro and ex vivo.Medical oncology (Northwood, London, England) · 2026Article
- Drug resistance in chronic myeloid leukemia: the involvement of Galectin-1 and Galectin-3.Molecular biology reports · 2026Review
- PRMT1 Promotes the Self-renewal of Leukemia Stem Cells by Regulating Protein Synthesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Mechanisms to medicines: navigating drug repurposing strategies in Alzheimer's disease.Frontiers in aging neuroscience · 2025Review
- The role of the lysine histone methylase KMT2D in chronic myeloid leukemia.Frontiers in pharmacology · 2025Article
- Review
- Molecular biomarkers of leukemia: convergence-based drug resistance mechanisms in chronic myeloid leukemia and myeloproliferative neoplasms.Frontiers in pharmacology · 2024Review
- Mechanisms underlying therapeutic resistance of tyrosine kinase inhibitors in chronic myeloid leukemia.International journal of biological sciences · 2024Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The hematopoietic neoplasm chronic myeloid leukemia (CML) is a rare disease caused by chromosomal reciprocal translocation t(9;22)(q34:q11) with subsequent formation of the BCR-ABL1 fusion gene. This fusion gene encodes a constitutively active tyrosine kinase, which results in malignant transformation of the cells. Since 2001, CML can be effectively treated using tyrosine kinase inhibitors (TKIs) such as imatinib, which prevent phosphorylation of downstream targets by blockade of the BCR-ABL kinase. Due to its tremendous success, this treatment became the role model of targeted therapy in precision oncology. Here, we review the mechanisms of TKI resistance focusing on BCR-ABL1-dependent and -independent mechanisms. These include the genomics of the BCR-ABL1, TKI metabolism and transport and alternative signaling pathways.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.