Jones Dan, Kamel-Reid Suzanne, Bahler David, Dong Henry, Elenitoba-Johnson Kojo, Press Richard, Quigley Neil, Rothberg Paul, Sabath Dan, Viswanatha David, Weck Karen, Zehnder James
ABL Mutation Working Group of the Association for Molecular Pathology, Clinical Practice Committee, Houston, Texas; University of Texas M. D. Anderson Cancer Center, Houston, Texas.
ABL Mutation Working Group of the Association for Molecular Pathology, Clinical Practice Committee, Houston, Texas; The University Health Network, Toronto, Canada.
J Mol Diagn. 2009 Jan;11(1):4-11. doi: 10.2353/jmoldx.2009.080095. Epub 2008 Dec 18.
The BCR-ABL tyrosine kinase produced by the t(9;22)(q34;q11) translocation, also known as the Philadelphia chromosome, is the initiating event in chronic myeloid leukemia (CML) and Ph+ acute lymphoblastic leukemia (ALL). Targeting of BCR-ABL with tyrosine kinase inhibitors (TKIs) has resulted in rapid clinical responses in the vast majority of patients with CML and Philadelphia chromosome+ ALL. However, long-term use of TKIs occasionally results in emergence of therapy resistance, in part through the selection of clones with mutations in the BCR-ABL kinase domain. We present here an overview of the current practice in monitoring for such mutations, including the methods used, the clinical and laboratory criteria for triggering mutational analysis, and the guidelines for reporting BCR-ABL mutations. We also present a proposal for a public database for correlating mutational status with in vitro and in vivo responses to different TKIs to aid in the interpretation of mutation studies.
由t(9;22)(q34;q11)易位产生的BCR-ABL酪氨酸激酶,也被称为费城染色体,是慢性髓性白血病(CML)和Ph+急性淋巴细胞白血病(ALL)的起始事件。用酪氨酸激酶抑制剂(TKIs)靶向BCR-ABL已在绝大多数CML和费城染色体阳性ALL患者中产生了快速的临床反应。然而,长期使用TKIs偶尔会导致治疗耐药性的出现,部分原因是通过选择BCR-ABL激酶结构域发生突变的克隆。我们在此概述当前监测此类突变的实践,包括所使用的方法、触发突变分析的临床和实验室标准,以及报告BCR-ABL突变的指南。我们还提出了一个公共数据库的建议,用于将突变状态与对不同TKIs的体外和体内反应相关联,以帮助解释突变研究。