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High expression of SLC38A1 predicts poor prognosis in patients with de novo acute myeloid leukemia
Author(s) -
Li Yan,
Shao Haigang,
Da Zhenzhen,
Pan Jinlan,
Fu Bin
Publication year - 2019
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.28632
Subject(s) - npm1 , myeloid leukemia , medicine , oncology , glutamine , biomarker , incidence (geometry) , myeloid , malignancy , cancer research , gene , karyotype , biology , amino acid , chromosome , genetics , physics , optics
The glutamine amino acid transporter solute carrier family 38 member 1 ( SLC38A1 ) is associated with the occurrence and progression of solid tumors. However, it has not yet been assessed in patients with hematologic malignancy. Herein, we investigated SLC38A1 expression and explored its clinical implications in acute myeloid leukemia (AML). The results showed that patients with high SLC38A1 expression had a lower mutation rate of NPM1 gene and higher incidence of adverse‐risk karyotype ( p = 0.0010 and 0.0051, respectively). Patients with a high level of SLC38A1 expression presented significantly shorter overall survival in whole‐cohort, chemotherapy‐only, and non‐inv(16) AML ( p = 0.0049, 0.0247, and 0.0005 respectively). Moreover, both univariate and multivariate analyses showed that high SLC38A1 expression was an independent unfavorable prognostic biomarker for AML ( p = 0.0057 and 0.0483, respectively). In summary, our study revealed SLC38A1 as a valuable prognostic and predictive marker for AML. Further, glutamine transporter SLC38A1 might serve as a potential target for the development of novel therapeutic drugs in the treatment of AML.