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BCR-ABL fusion transcript types and levels and their interaction with secondary genetic changes in determining the phenotype of Philadelphia chromosome-positive leukemias.BCR-ABL融合转录本类型、水平及其在决定费城染色体阳性白血病表型过程中与继发性基因改变的相互作用。
Blood. 2008 Dec 15;112(13):5190-2. doi: 10.1182/blood-2008-04-148791. Epub 2008 Sep 22.
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ABL kinase domain pseudoexon insertion is not uncommon in BCR-ABL transcripts.
J Mol Diagn. 2008 Sep;10(5):475-6; author reply 476. doi: 10.2353/jmoldx.2008.080055. Epub 2008 Aug 7.
3
Kinase domain point mutations in Philadelphia chromosome-positive acute lymphoblastic leukemia emerge after therapy with BCR-ABL kinase inhibitors.费城染色体阳性急性淋巴细胞白血病中的激酶结构域点突变在使用BCR-ABL激酶抑制剂治疗后出现。
Cancer. 2008 Sep 1;113(5):985-94. doi: 10.1002/cncr.23666.
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Absolute quantitative detection of ABL tyrosine kinase domain point mutations in chronic myeloid leukemia using a novel nanofluidic platform and mutation-specific PCR.使用新型纳米流体平台和突变特异性PCR对慢性髓性白血病中ABL酪氨酸激酶结构域点突变进行绝对定量检测。
Leukemia. 2009 Feb;23(2):396-9. doi: 10.1038/leu.2008.183. Epub 2008 Jul 10.
5
ACMG recommendations for standards for interpretation and reporting of sequence variations: Revisions 2007.美国医学遗传学与基因组学学会(ACMG)关于序列变异解读和报告标准的建议:2007年修订版
Genet Med. 2008 Apr;10(4):294-300. doi: 10.1097/GIM.0b013e31816b5cae.
6
Characteristics and outcomes of patients with chronic myeloid leukemia and T315I mutation following failure of imatinib mesylate therapy.甲磺酸伊马替尼治疗失败后慢性髓性白血病伴T315I突变患者的特征及转归
Blood. 2008 Jul 1;112(1):53-5. doi: 10.1182/blood-2007-11-123950. Epub 2008 Apr 10.
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Characterization of BCR-ABL deletion mutants from patients with chronic myeloid leukemia.慢性髓性白血病患者BCR-ABL缺失突变体的特征分析
Leukemia. 2008 Jun;22(6):1184-90. doi: 10.1038/leu.2008.65. Epub 2008 Mar 20.
8
An intron-derived insertion/truncation mutation in the BCR-ABL kinase domain in chronic myeloid leukemia patients undergoing kinase inhibitor therapy.接受激酶抑制剂治疗的慢性髓性白血病患者中,BCR-ABL激酶结构域存在内含子衍生的插入/截断突变。
J Mol Diagn. 2008 Mar;10(2):177-80. doi: 10.2353/jmoldx.2008.070128. Epub 2008 Feb 14.
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Monitoring treatment of chronic myeloid leukemia.监测慢性髓性白血病的治疗。
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10
RUNX1 DNA-binding mutations and RUNX1-PRDM16 cryptic fusions in BCR-ABL+ leukemias are frequently associated with secondary trisomy 21 and may contribute to clonal evolution and imatinib resistance.BCR-ABL+白血病中的RUNX1 DNA结合突变和RUNX1-PRDM16隐匿性融合常与继发性21三体相关,并可能促进克隆进化和伊马替尼耐药。
Blood. 2008 Apr 1;111(7):3735-41. doi: 10.1182/blood-2007-07-102533. Epub 2008 Jan 17.

慢性粒细胞白血病和急性淋巴细胞白血病中检测及报告BCR-ABL耐药突变的实验室实践指南:分子病理学协会报告

Laboratory practice guidelines for detecting and reporting BCR-ABL drug resistance mutations in chronic myelogenous leukemia and acute lymphoblastic leukemia: a report of the Association for Molecular Pathology.

作者信息

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

机构信息

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.

出版信息

J Mol Diagn. 2009 Jan;11(1):4-11. doi: 10.2353/jmoldx.2009.080095. Epub 2008 Dec 18.

DOI:
10.2353/jmoldx.2009.080095
PMID:19095773
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2607559/
Abstract

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.

摘要

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。