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.
题目: BCR-ABLT315I突变与慢性粒细胞白血病治疗研究的最新进展.
摘要: BCR-ABLT315I突变是导致慢性粒细胞白血病（CML）患者对第一、二代酪氨酸激酶抑制剂（TKI）耐药的主要 机制。研究发现，第三代TKI Ponatinib可明显改善T315I突变导致耐药的CML患者的预后，但最新报道的T315I复合突变体甚至对Ponatinib也耐药，再度激发了人们对CML耐药机制和靶向治疗的研究热情。既往研究表明，TKI联合其他靶向药物对由T315I突变而导致耐药或复发的CML患者有效。最新研究发现，变构抑制剂Asciminib联合TKI治疗对携带T315I复合突变的CML患者同样有效，但具体机制尚未明确。本文将围绕BCR-ABLT315I突变与CML治疗研究的最新进展进行综述，期望为临床针对T315I突变CML的新药研发和改进治疗提供参考。.
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