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Updated: Jul 21, 2026
A Method for Screening and Validation of Resistant Mutations Against Kinase Inhibitors
Published on: December 7, 2014
[Recent Advance of Newly Therapy for Chronic Myeloid Leukemia with BCR-ABL Mutation--Review]
Hu-Rong Lai1,2, Qian-Miao Wu1,2, Ya-Zhi Yang1,2
1Key Laboratory of Hematology, The Second Affiliated Hospital of Nanchang University.
Abstract:
BCR-ABL mutation is the main mechanism of resistance to the first and second generation tyrosine kinase inhibitor (TKI) for patients with chronic myeloid leukemia (CML). Ponatinib as the third generation TKI has been found that can significantly improve the prognosis of CML patients with T315I mutation. However, the latest report has discovered that the T315I compound mutant is even resistant to ponatinib, which aroused the enthusiasm of research on the mechanism of CML resistance and targeted therapy once again. Previous studies have shown that TKI combined with other targeted drugs is effective to CML patients with drug resistance or relapse due to T315I mutation. The latest research has found that the allosteric inhibitor asciminib combined with TKI therapy is equally effective to CML patients with T315I compound mutant, but the specific mechanism is not yet clarified. This review will focus on the latest research progress of therapy for CML with BCR-ABL mutation, hoping to provide reference for researching new drugs and improve therapy for treating CML with T315I mutation.
Insights
Resistance to tyrosine kinase inhibitors (TKIs) in chronic myeloid leukemia (CML) is often due to BCR-ABL mutations. New combination therapies show promise for treating CML patients with resistant T315I mutations.
Area of Science:
- Oncology
- Hematology
- Molecular Biology
Background:
- BCR-ABL mutations are a primary cause of resistance to tyrosine kinase inhibitors (TKIs) in chronic myeloid leukemia (CML).
- Third-generation TKI, ponatinib, is effective for CML with T315I mutations, but resistance to ponatinib has emerged.
- Compound T315I mutations present a new challenge, necessitating novel therapeutic strategies for CML.
Conclusions:
- Targeted therapies and combination treatments are crucial for overcoming BCR-ABL mediated TKI resistance in CML.
- Asciminib offers a potential new avenue for treating CML patients with challenging T315I compound mutations.
- Continued research into CML resistance mechanisms and novel drug combinations is essential for improving patient outcomes.
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