KIT mutations correlate with adverse survival in children with core-binding factor acute myeloid leukemia

Xi ChenCenter for Clinical Molecular Medicine, Children’s Hospital of Chongqing Medical University, Chongqing, China; ;Ministry of Education Key Laboratory of Child Development and Disorders, Children’s Hospital of Chongqing Medical University, Chongqing, China; ;Chongqing Key Laboratory of Pediatrics, Children’s Hospital of Chongqing Medical University, Chongqing, China;

Hu DouMinistry of Education Key Laboratory of Child Development and Disorders, Children’s Hospital of Chongqing Medical University, Chongqing, China; ;Department of Clinical Laboratory, Children’s Hospital of Chongqing Medical University, Chongqing, China; ;Key Laboratory of Pediatrics in Chongqing, Children’s Hospital of Chongqing Medical University, Chongqing, China; ;Chongqing International Science and Technology Cooperation Center for Child Development and Disorders, Children’s Hospital of Chongqing Medical University, Chongqing, China;

Xingjuan WangCenter for Clinical Molecular Medicine, Children’s Hospital of Chongqing Medical University, Chongqing, China; ;Ministry of Education Key Laboratory of Child Development and Disorders, Children’s Hospital of Chongqing Medical University, Chongqing, China; ;Chongqing Key Laboratory of Pediatrics, Children’s Hospital of Chongqing Medical University, Chongqing, China;

Yi HuangMinistry of Education Key Laboratory of Child Development and Disorders, Children’s Hospital of Chongqing Medical University, Chongqing, China; ;Chongqing Key Laboratory of Pediatrics, Children’s Hospital of Chongqing Medical University, Chongqing, China; ;Research Center for Immunity and Infectious Diseases, Children’s Hospital of Chongqing Medical University, Chongqing, China;

Ling LuDepartment of Rheumatology, Huashan Hospital, Fudan University, Shanghai, China;

Junqing BinCenter for Clinical Molecular Medicine, Children’s Hospital of Chongqing Medical University, Chongqing, China; ;Ministry of Education Key Laboratory of Child Development and Disorders, Children’s Hospital of Chongqing Medical University, Chongqing, China; ;Chongqing Key Laboratory of Pediatrics, Children’s Hospital of Chongqing Medical University, Chongqing, China;

Yongchun SuMinistry of Education Key Laboratory of Child Development and Disorders, Children’s Hospital of Chongqing Medical University, Chongqing, China; ;Chongqing Key Laboratory of Pediatrics, Children’s Hospital of Chongqing Medical University, Chongqing, China; ;Department of Hematology and Oncology, Children’s Hospital of Chongqing Medical University, Chongqing, China;

Lin ZouCenter for Clinical Molecular Medicine, Children’s Hospital of Chongqing Medical University, Chongqing, China; ;Ministry of Education Key Laboratory of Child Development and Disorders, Children’s Hospital of Chongqing Medical University, Chongqing, China; ;Chongqing Key Laboratory of Pediatrics, Children’s Hospital of Chongqing Medical University, Chongqing, China;

Jie YuMinistry of Education Key Laboratory of Child Development and Disorders, Children’s Hospital of Chongqing Medical University, Chongqing, China; ;Chongqing Key Laboratory of Pediatrics, Children’s Hospital of Chongqing Medical University, Chongqing, China; ;Department of Hematology and Oncology, Children’s Hospital of Chongqing Medical University, Chongqing, China; Correspondence[email protected]

Liming BaoDepartment of Pathology and Laboratory Medicine, Geisel School of Medicine at Dartmouth College, Hanover, NH, USACorrespondence[email protected]

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Abstract

The prevalence and clinical relevance of KIT mutations in childhood core-binding factor (CBF) acute myeloid leukemia (AML) have not been well characterized. In this study, a total of 212 children with de novo AML were enrolled from a Chinese population and 50 (23.5%) of the patients were deemed CBF-AML. KIT mutations were identified in 30% of the CBF-AML cohort. The KIT mutations were clustered in exon 17 and exon 8, and KIT mutations in exons 8 and 17 were correlated with a shorter overall survival (OS) (5-year OS: 30.0 ± 14.5% vs. 73.0 ± 8.5%, p = .007) and event-free survival (EFS) (5-year EFS: 30.0 ± 14.5% vs. 73.0 ± 8.5%, p = .003). Multivariate analysis revealed KIT mutations as an independent risk factor in CBF-AML. Our results suggest that KIT mutations are a molecular marker for an inferior prognosis in pediatric CBF-AML.

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Acknowledgements

The authors are indebted to the patients, families, and physicians for their participation in the study. The study was supported in part by a grant from the Children’s Hospital of Chongqing Medical University [Grant No. ZHYX2013-7], and a grant from the Science and Technology Commission of Chongqing Municipality [Grant No. cstc2016jcyjA0330].

Potential conflict of interest

Disclosure forms provided by the authors are available with the full text of this article online at https://doi.org/10.1080/10428194.2017.1361025.

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KIT mutations correlate with adverse survival in children with core-binding factor acute myeloid leukemia

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KIT mutations correlate with adverse survival in children with core-binding factor acute myeloid leukemia

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