The DOI matches its Crossref record; 166 of the 175 references it cites were found in a registry or an index.
Resistance to Tyrosine Kinase Inhibition Therapy for Chronic Myelogenous Leukemia: A Clinical Perspective and Emerging Treatment Options
Open accessAbstract
The development of tyrosine kinase inhibitors (TKIs) has led to extended lifespans for many patients with chronic myelogenous leukemia (CML). However, 20% to 30% of patients fail to respond, respond suboptimally, or experience disease relapse after treatment with imatinib. A key factor is drug resistance. The molecular mechanisms implicated in this resistance include those that involve upregulation or mutation of BCR-ABL kinase and those that are BCR-ABL independent. The clinical consequences of these molecular mechanisms of resistance for disease pathogenesis remain open for debate. This review summarizes the molecular mechanisms and clinical consequences of TKI resistance and addresses the current and future treatment approaches for patients with TKI-resistant CML.
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“One cluster summarized the concepts related to the development of resistance to chemotherapy drugs, rendering the treatment ineffective in inhibiting cancer cell proliferation or inducing cell death. This discovery has been repeatedly validated through experimental results from BCR-ABL kinase-independent pathways that promote CML cell survival and proliferation, bypassing TKI inhibition [84, 85].”
From GOLDEN fusion: a graph-oriented learning with domain-embedding network fusion for generating super gene sets in functional genomics (2026) · cites this paper as [85]
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O’Brien, S. G., Guilhot, F., Larson, R. A., Gathmann, I., Baccarani, M., Cervantes, F., Cornelissen, J. J., Fischer, T. H., Hochhaus, A., Hughes, T. P., et al. (2003) · New England Journal of Medicine · doi:10.1056/nejmoa022457 · Cited by 3,550
Self-citationFive-Year Follow-up of Patients Receiving Imatinib for Chronic Myeloid Leukemia
Druker, B. J., Guilhot, F., O’Brien, S. G., Gathmann, I., Kantarjian, H. M., Gattermann, N., Deininger, M. W., Silver, R. T., Goldman, J. M., Stone, R. M., et al. (2006) · New England Journal of Medicine · doi:10.1056/nejmoa062867 · Cited by 3,516
Self-citationClinical Resistance to STI-571 Cancer Therapy Caused by BCR-ABL Gene Mutation or Amplification
Gorre, M. E., Mohammed, M., Ellwood, K., Hsu, N., Paquette, R., Rao, P. N., & Sawyers, C. L. (2001) · Science · doi:10.1126/science.1062538 · Cited by 3,104
Hematologic and Cytogenetic Responses to Imatinib Mesylate in Chronic Myelogenous Leukemia
Kantarjian, H., Sawyers, C. L., Hochhaus, A., Guilhot, F., Schiffer, C. A., Gambacorti-Passerini, C. B., Niederwieser, D. W., Resta, D. J., Capdeville, R., Zoellner, U., et al. (2002) · New England Journal of Medicine · doi:10.1056/nejmoa011573 · Cited by 2,005
Self-citationStructural Mechanism for STI-571 Inhibition of Abelson Tyrosine Kinase
Schindler, T. H., Bornmann, W. G., Pellicena, P., Miller, W. T., Clarkson, B., & Kuriyan, J. (2000) · Science · doi:10.1126/science.289.5486.1938 · Cited by 1,785
Dasatinib in imatinib-resistant Philadelphia chromosome-positive leukemias
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Characterization of AMN107, a selective inhibitor of native and mutant Bcr-Abl
Weisberg, E., Manley, P. W., Breitenstein, W., Brüggen, J., Cowan‐Jacob, S. W., Ray, A., Huntly, B. J. P., Fabbro, D., Fendrich, G., Hall–Meyers, E., et al. (2005) · Cancer Cell · doi:10.1016/j.ccr.2005.01.007 · Cited by 1,509
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9 of the 175 references couldn’t be matched to a known paper.
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- Hochhaus, 2012, Blood, 120
- Cortes, 2012, Blood, 120
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Okabe, S., Arai, Y., & Gotoh, A. (2024) · Discover Oncology · doi:10.1007/s12672-024-01706-6
Unveiling Targeted Approaches to Combat Drug Resistance in Cancer Chemotherapy
Siddharth, Siddhant, Salahuddin, Mazumder, A., Kumar, R., & Debnath, A. (2025) · Current Pharmaceutical Design · doi:10.2174/0113816128380235250627143945
Sy, S. K. B., Yoon, D. Y., Yang, Y., Darstein, C., Dasgupta, K., Kapoor, S., Wu, S., Kawakita, Y., Hoch, M., & Grosch, K. (2026) · Clinical Pharmacokinetics · doi:10.1007/s40262-025-01616-y
Metadata
- Authors
- Jabbour, E. J., Cortes, J. E., & Kantarjian, H. M.
- Affiliations
- The University of Texas MD Anderson Cancer Center (US)
- Corresponding author
- Jabbour, Elias J.
- Venue
- Clinical Lymphoma Myeloma and Leukemia
- Publisher
- Elsevier BV
- Published
- 2013-10
- Volume
- 13
- Issue
- 5
- Pages
- 515-529
- ISSN
- 2152-2650 (ISSN-L)
- PMC
- PMC4160831
- OpenAlex
- W2064888584
- Cited by
- 105
- References
- 175
- Citations by year
- 2026: 2 · 2025: 5 · 2024: 8 · 2023: 3 · 2022: 13 · 2021: 12 · 2020: 8 · 2019: 11 · 2018: 5 · 2017: 8 · 2016: 5 · 2015: 19 · 2014: 6
- FWCI
- 1.52
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Clinical Lymphoma Myeloma & Leukemia (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Anthemis Consulting Ltd.
- Teva Pharmaceutical Industries
- Bristol-Myers Squibb
- Novartis
- Ariad
- Pfizer
- ChemGenex
- Topics
- Health Sciences › Medicine › Hematology › Chronic Myeloid Leukemia Treatments
- Health Sciences › Medicine › Hematology › Chronic Lymphocytic Leukemia Research
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Treatments and Mutations
- Keywords
- chronic myeloid leukemia, tyrosine kinase inhibitors, imatinib, drug resistance, BCR-ABL tyrosine kinase, recurrence, second-line therapy, molecular mechanisms of resistance
- MeSH terms
- Antineoplastic Agents, Humans, Mutation, Leukemia, Myelogenous, Chronic, BCR-ABL Positive, Fusion Proteins, bcr-abl, Treatment Outcome, Drug Resistance, Neoplasm, Amino Acid Substitution, Protein Kinase Inhibitors
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