Utility of IDH1/2 mutations as biomarkers for detection of measurable residual disease in acute myeloid leukemia

IDH1/2突变作为急性髓系白血病中可测量残留病灶检测生物标志物的应用

阅读:1

Abstract

Molecular measurable residual disease (MRD) assessment in patients with acute myeloid leukemia (AML) has been established for only a few specific markers: mutant NPM1 and FLT3 internal tandem duplication (ITD). Mutations in isocitrate dehydrogenase 1 (IDH1) and isocitrate dehydrogenase 2 (IDH2) are present in ∼20% of patients with AML. However, validation of mutant IDH1/2 MRD has been hampered by cohort size as well as the availability of highly sensitive and specific MRD detection assays. Here, we comprehensively investigate the impact of persistent IDH1/2 mutations in complete remission after intensive chemotherapy in a cohort of 163 newly diagnosed patients with IDH-mutant AML, enrolled in Dutch-Belgian Cooperative Trial Group for Hematology-Oncology and Swiss Group for Clinical Cancer Research clinical trials, using a next-generation sequencing (NGS)-based approach, targeting all hot spot mutations in IDH1 (R132) and IDH2 (R140 and R172). The high sensitivity (10-4) as well as the levels of persistent IDH1/2 mutations detected by the NGS-based approach were confirmed by an independent super rolling circle amplification assay. We demonstrate that the risk of relapse was significantly increased in patients with AML with measurable persistent IDH2 mutations (P = .027; subdistribution hazard ratio (SHR), 2.34) but not in patients with persistent mutant IDH1 (P = .591; SHR, 0.80). Moreover, the association of persistence of mutant IDH2 and increased risk of relapse was most pronounced in patients with mutant IDH2 AML without concomitant NPM1 mutations or FLT3-ITD (P = .011; SHR, 5.29). Thus, mutant IDH2 appears as a potentially useful novel molecular MRD marker with prognostic significance in AML.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。