Recent Advance of Newly Therapy for Chronic Myeloid Leukemia with BCR-ABLT315I Mutation--Review.
10.19746/j.cnki.issn.1009-2137.2023.05.052
- Author:
Hu-Rong LAI
1
;
Qian-Miao WU
1
;
Ya-Zhi YANG
1
;
Jian LI
2
Author Information
1. Key Laboratory of Hematology, The Second Affiliated Hospital of Nanchang University.
2. Key Laboratory of Hematology, The Second Affiliated Hospital of Nanchang University.E-mail: ndefy03048@ncu.edu.cn.
- Publication Type:Journal Article
- Keywords:
chronic myeloid leukemia;
drug resistance;
therapy advance;
tyrosine kinase inhibitor
- MeSH:
Humans;
Drug Resistance, Neoplasm/genetics*;
Leukemia, Myelogenous, Chronic, BCR-ABL Positive/genetics*;
Fusion Proteins, bcr-abl/genetics*;
Protein Kinase Inhibitors/therapeutic use*;
Mutation;
Antineoplastic Agents/pharmacology*
- From:
Journal of Experimental Hematology
2023;31(5):1579-1583
- CountryChina
- Language:Chinese
-
Abstract:
BCR-ABLT315I 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-ABLT315I mutation, hoping to provide reference for researching new drugs and improve therapy for treating CML with T315I mutation.
