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High expression of SLC38A1 predicts poor prognosis in patients with de novo acute myeloid leukemia

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 impl...

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Bibliographic Details
Published in:Journal of cellular physiology 2019-11, Vol.234 (11), p.20322-20328
Main Authors: Li, Yan, Shao, Haigang, Da, Zhenzhen, Pan, Jinlan, Fu, Bin
Format: Article
Language:English
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Summary: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. This is the first report about the solute carrier family 38 member 1 (SLC38A1) expression with the outcome of acute myeloid leukemia (AML) patients. The results confirmed that the high expression of SLC38A1 was an adverse prognostic indicator for AML.
ISSN:0021-9541
1097-4652
DOI:10.1002/jcp.28632