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[Cancer Research 66, 3310-3316, March 15, 2006]
© 2006 American Association for Cancer Research

Clinical Research

Nucleophosmin Mutations in De novo Acute Myeloid Leukemia: The Age-Dependent Incidences and the Stability during Disease Evolution

Wen-Chien Chou1,2, Jih-Luh Tang1, Liang-In Lin4, Ming Yao1, Woei Tsay1, Chien-Yuan Chen1, Shang-Ju Wu1, Chi-Fei Huang1, Rong-Jing Chiou1, Mei-Hsuan Tseng1, Dong-Tsamn Lin2,3, Kai-Hsin Lin3, Yao-Chang Chen1,2 and Hwei-Fang Tien1

Departments of 1 Internal Medicine, 2 Laboratory Medicine, and 3 Pediatrics, National Taiwan University Hospital; and 4 Graduate Institute of Medical Technology, National Taiwan University, Taipei, Taiwan

Requests for reprints: Hwei-Fang Tien, Department of Internal Medicine, National Taiwan University Hospital, 100 Taipei, Taiwan. Phone: 886-2-23123456, ext. 3955; Fax: 886-2-23959583; E-mail: hftd{at}ha.mc.ntu.edu.tw.

Nucleophosmin (NPM) mutations have been found in a significant proportion of adults with de novo acute myeloid leukemia (AML), especially in those of a normal karyotype. These results provide a basis for studies of the pathogenesis in this specific subgroup of AML. In this study, NPM mutations were analyzed in 173 Chinese patients of de novo AML, including adults and children. We found that NPM mutations were present in 19.1% of the overall population and 40.3% of those with a normal karyotype. Adults had a significantly higher incidence of NPM mutations than children [32 of 126 (25.4%) versus 1 of 47 (2.1%), P < 0.001]. NPM mutations were closely associated with normal karyotype (P < 0.001) and internal tandem duplication of FLT3 (P = 0.002), but negatively associated with CEBPA mutations (P = 0.032) and expression of CD34 (P < 0.001) and HLA-DR (P = 0.003). Serial analyses of NPM mutations showed the mutation disappeared at complete remission, but the same mutation reappeared at relapse, except for one who lost the mutation at the second relapse, when new cytogenetic abnormalities emerged. None acquired novel mutations during the follow-up period. In conclusion, NPM mutations occur in an age-dependent fashion. Moreover, the findings that NPM mutations are stable during disease evolution and closely associated with disease status make it a potential marker for monitoring minimal residual disease. (Cancer Res 2006; 66(6): 3310-6)




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