Cited by 105Chronic Myeloid Leukemia TreatmentsChronic Lymphocytic Leukemia ResearchLung Cancer Treatments and Mutations

Resistance to tyrosine kinase inhibition therapy for chronic myelogenous leukemia: a clinical perspective and emerging treatment options

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Jabbour, Elias J., Cortes, Jorge E., Kantarjian, Hagop M.·2013·Clinical Lymphoma Myeloma and Leukemia

Abstract

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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Crossref · 10.1016/j.clml.2013.03.018

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  • One cluster in the CML case study summarized concepts related to the development of resistance to chemotherapy drugs, rendering the treatment ineffective in inhibiting cancer cell proliferation or inducing cell death.

    “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]

    The sections on alternative signaling pathways and stem-cell persistence report BCR-ABL-independent mechanisms by which CML cells survive imatinib treatment, with cytokine support permitting growth. The paper describes the Src pathway as one that “seems” critical and says the clinical significance of some resistance mechanisms remains under investigation; it does not establish the citing sentence’s stronger claim of repeated experimental validation. (LLM, conf=0.82)

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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)
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
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 › Genetics › 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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