ReviewFrontiers in pharmacology2021
Pharmacogenomics of Impaired Tyrosine Kinase Inhibitor Response: Lessons Learned From Chronic Myelogenous Leukemia.
Review in Frontiers in pharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- Structure and Dynamics of the ABL1 Tyrosine Kinase and Its Important Role in Chronic Myeloid Leukemia.Archiv der Pharmazie · 2025Review
- Association of fibronectin 1 deregulation with tyrosine kinase inhibitor resistance in chronic myeloid leukemia.Frontiers in cell and developmental biology · 2025Article
- A novel imatinib analogue inhibitor of chronic myeloid leukaemia: design, synthesis and characterization-explanation of its folded conformation.Royal Society open science · 2025Article
- BTK acts as a modulator of the response to imatinib in chronic myeloid leukemia.Oncology letters · 2024Article
- Alterations in pharmacogenetic genes and their implications for imatinib resistance in Chronic Myeloid Leukemia patients from an admixed population.Cancer chemotherapy and pharmacology · 2024Article
- PROteolysis-Targeting Chimeras (PROTACs) in leukemia: overview and future perspectives.MedComm · 2024Review
- Moving toward precision medicine to predict drug sensitivity in patients with metastatic breast cancer.ESMO open · 2024Review
- Mechanisms underlying therapeutic resistance of tyrosine kinase inhibitors in chronic myeloid leukemia.International journal of biological sciences · 2024Review
- Which Second-Line Tyrosine Kinase Inhibitor(s) for Chronic Myeloid Leukemia?Current treatment options in oncology · 2023Review
- Dose Optimization in Oncology Drug Development: The Emerging Role of Pharmacogenomics, Pharmacokinetics, and Pharmacodynamics.Cancers · 2023Review
- Role of Turmeric and Curcumin in Prevention and Treatment of Chronic Diseases: Lessons Learned from Clinical Trials.ACS pharmacology & translational science · 2023Review
- A customized mass array panel forJournal of mass spectrometry and advances in the clinical lab · 2023Article
- Clonal evolution in tyrosine kinase inhibitor-resistance: lessons fromFrontiers in oncology · 2023Article
- The 10th Santorini conference: Systems medicine, personalised health and therapy. "The odyssey from hope to practice: Patient first.Frontiers in genetics · 2023Article
- Carnosine Potentiates Doxorubicin-Induced Cytotoxicity in Resistant NCI/ADR-RES Cells by Inhibiting P-Glycoprotein-In Silico and In Vitro Evidence.Molecules (Basel, Switzerland) · 2022Article
- Comparative Assessment of Quantification Methods for Tumor Tissue Phosphoproteomics.Analytical chemistry · 2022Article
- Article
- Targeted Therapies in Cancer: To Be or Not to Be, Selective.Biomedicines · 2021Review
- Resistance to Tyrosine Kinase Inhibitors in Chronic Myeloid Leukemia-From Molecular Mechanisms to Clinical Relevance.Cancers · 2021Review
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Authors and funding
2 authors.
Funding
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Abstract
The use of small molecules became one key cornerstone of targeted anti-cancer therapy. Among them, tyrosine kinase inhibitors (TKIs) are especially important, as they were the first molecules to proof the concept of targeted anti-cancer treatment. Since 2001, TKIs can be successfully used to treat chronic myelogenous leukemia (CML). CML is a hematologic neoplasm, predominantly caused by reciprocal translocation t(9;22)(q34;q11) leading to formation of the so-called BCR-ABL1 fusion gene. By binding to the BCR-ABL1 kinase and inhibition of downstream target phosphorylation, TKIs, such as imatinib or nilotinib, can be used as single agents to treat CML patients resulting in 80 % 10-year survival rates. However, treatment failure can be observed in 20-25 % of CML patients occurring either dependent or independent from the BCR-ABL1 kinase. Here, we review approved TKIs that are indicated for the treatment of CML, their side effects and limitations. We point out mechanisms of TKI resistance focusing either on BCR-ABL1-dependent mechanisms by summarizing the clinically observed BCR-ABL1-mutations and their implications on TKI binding, as well as on BCR-ABL1-independent mechanisms of resistances. For the latter, we discuss potential mechanisms, among them cytochrome P450 implications, drug efflux transporter variants and expression, microRNA deregulation, as well as the role of alternative signaling pathways. Further, we give insights on how TKI resistance could be analyzed and what could be learned from studying TKI resistance in CML
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