Is there a cloud in the silver lining for imatinib?
2003
Understanding Imatinib Resistance in Chronic Myeloid Leukaemia
publication
Evidence: moderate
Author Information
Author(s): Paterson S C, Smith K D, Holyoake T L, Jørgensen H G
Hypothesis
What mechanisms contribute to resistance against imatinib in chronic myeloid leukaemia patients?
Conclusion
Various mechanisms, including gene amplification and mutations, contribute to resistance against imatinib in chronic myeloid leukaemia.
Supporting Evidence
- BCR-ABL gene amplification has been observed in some CML patients who relapsed after initially responding to imatinib.
- Point mutations in the BCR-ABL gene can alter the drug-binding pocket, leading to resistance.
- Quiescent Ph+ stem cells in CML patients are resistant to imatinib, complicating treatment.
Takeaway
Some patients with chronic myeloid leukaemia may stop responding to a drug called imatinib because their cancer cells change in ways that make the drug less effective.
Limitations
The findings may not be representative due to the small number of patients analyzed.
Digital Object Identifier (DOI)
Want to read the original?
Access the complete publication on the publisher's website