Treatment and molecular monitoring update in chronic myeloid leukemia management

被引:8
|
作者
Sorel, Nathalie [1 ]
Cayssials, Emilie [2 ]
Brizard, Francoise [3 ]
Chomel, Jean-Claude [1 ]
机构
[1] CHU Poitiers, Serv Cancerol Biol, Poitiers, France
[2] CHU Poitiers, Serv Oncol Hematol & Therapie Cellulaire, Poitiers, France
[3] CHU Poitiers, Serv Hematol Biol, Poitiers, France
关键词
chronic myeloid leukemia; tyrosine kinase inhibitors; molecular monitoring; BCR-ABL1; resistance; CHRONIC MYELOGENOUS LEUKEMIA; TYROSINE KINASE INHIBITORS; BCR-ABL1 COMPOUND MUTATIONS; RESIDUAL DISEASE DETECTION; POLYMERASE-CHAIN-REACTION; BCR-ABL INHIBITORS; 3-YEAR FOLLOW-UP; CML PATIENTS; STEM-CELLS; EUROPEAN LEUKEMIANET;
D O I
10.1684/abc.2017.1233
中图分类号
R446 [实验室诊断]; R-33 [实验医学、医学实验];
学科分类号
1001 ;
摘要
Chronic myeloid leukemia (CML) is a myeloproliferative neoplasm resulting from the t( 9; 22)(q34; q11) translocation. It is characterized by the presence of the BCR-ABL1 fusion gene encoding the BCR-ABL oncoprotein characterized by a deregulated tyrosine kinase activity. Targeted therapies using tyrosine kinase inhibitors (TKI) such as imatinib, dasatinib, nilotinib, bosutinib, or ponatinib have profoundly changed the natural history of the disease with a major impact on survival. Indeed, most patients diagnosed today can enjoy a near normal life expectancy. The efficacy of TKI treatment can be accurately evaluated by a molecular monitoring based on the quantification of BCR-ABL1 mRNA transcripts and the detection of resistance mutations in the BCR-ABL kinase domain. International recommendations for an optimal management of CML using biological parameters are regularly published. They were designed to evaluate the response to the treatment and to consider, if necessary, a switch to another TKI. A sustained and deep molecular response is obtained in a significant percentage of patients. Clinical trials of TKI discontinuation were performed in such a population, and half of patients do not relapse. In the remaining patients, a rapid appearance of the malignant clone was observed, undoubtedly the consequence of the persistence of residual leukemic stem cells (LSCs). How to discriminate patients who may safely stop TKI? How to target residual LSCs, and do we have to eradicate all these cells? Additional research investigation and clinical trials are needed to answer these questions in order to consider a potential cure of CML.
引用
收藏
页码:129 / 145
页数:17
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