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Treatment selection after imatinib resistance in chronic myeloid leukemia

  • Elias Jabbour(corresponding author)
    ,
  • ,
  • Hagop Kantarjian
*Corresponding author for this work
  • University of Texas MD Anderson Cancer Center
Scholary Output:
Contribution to journal
Review article
Peer-review

Sustainable Development Goals

  • SDG 3 - Good Health and Well-being
    SDG 3 Good Health and Well

Abstract

Chronic myeloid leukemia (CML) is a progressive and often fatal malignancy of the blood. The harbinger of CML is a chromosomal translocation that results in the synthesis of the BCR-ABL fusion protein, a constitutively active tyrosine kinase. The advent of imatinib, an inhibitor targeted specifically for BCR-ABL, represented a significant medical advance in CML therapy. However, patients with CML can exhibit varying responses to first-line treatment with imatinib. While most patients respond to treatment, some may experience a loss of response or require treatment discontinuation due to toxicity. Frequent monitoring for resistance or intolerance is a requirement for recognition of suboptimal response. Mutational analysis of the patient's BCR-ABL alleles is also informative and may be predictive of a response to therapy. Published physician guidelines have highlighted these recommendations, but it is not clear if these guidelines are universally followed. One option in patients showing poor response to standard-dose imatinib of 400 mg is to escalate the dose. However, this option should be reserved for patients with minimal disease burden. Clinically available options mainly include second-generation tyrosine kinase inhibitors, such as dasatinib and nilotinib. Allogenic stem cell transplantations (for eligible patients) also should be considered. The disease and patient characteristics at the time of imatinib failure should be evaluated before choosing second-line therapy to optimize the therapeutic benefit without unnecessary delay.

Publication Information

Output type

Scholary Output:
Contribution to journal
Review article
Peer-review

Original language

English (US)

Pages from-to (Number of pages)

Pages 3-10 (8 pages)

Journal (Volume, Issue Number)

Targeted Oncology (Volume 4, Issue 1)

Publication milestones

  • Published - 01/2009

Publication status

Published - 01/2009

ISSN

1776-2596

Publication IDs

  • Scopus: 67349179696
  • PubMed: 19343297

Publication metrics

Metrics

SciVal
FWCI
1.47
SciVal
Author count
3
SciVal
citations
40
SciVal
Paper percentile
86
Scopus
citations
Fractional count
1
Fractional count
0.33
Fractional count
2
Fractional count
0.67
Fractional count
1
Fractional count
1

PlumX, opens in new tab

Captures
20
Citation count
47

Funding Details

Acknowledgement Editorial and writing support was provided by Gardiner-Caldwell U.S., funded by Bristol-Myers Squibb.