Abstract
Solute carrier family 38 member 1 (SLC38A1) is a principal glutamine transporter associated with solid tumor development and progression. However, it has rarely been investigated in hematologic malignancies. This study aimed to assess the expression status and correlation of SLC38A1 with clinicopathological features in acute leukemia patients. In this cross-sectional study, SLC38A1 expression was evaluated via RTQ-PCR in 140 denovo acute leukemia patients (70 adult AML cases and 70 pediatrics B-ALL cases) and 70 healthy controls (40 adults and 30 children for the AML and B-ALL groups, respectively). Statistical analysis was done by IBM SPSS software version 20. Other clinical and laboratory data including genetic testing, when available, were extracted from the Hospital Information System (HIS). We found that SLC38A1 was overexpressed in both types of acute leukemia patients compared with controls (Median (IQR): 4.26(11.32) for AML vs. 1.08(1.68) for control; P = 0.026, and 5.76(15.97) for B-ALL vs. 0.65(1.18) for control; P = 0.019). The distribution of FAB and WHO classifications varied significantly between AML patients with high SLC38A1 expression compared to those with low expression (P = 0.005 and P = 0.017, respectively). In addition, B-ALL patients in low or high SCL38A1 expression groups showed various distributions regarding WHO classification (P = 0.03). In Kaplan-Meier analysis, both AML and B-ALL patients with SLC38A1 (high) had shorter overall survival (OS) compared to SLC38A1 (low) patients (P < 0.001 and P = 0.007, respectively). Multivariate analysis confirmed that SLC38A1 upregulation was an independent indicator for prognosis in acute leukemia patients (HR = 3.856, 95% CI = 1.766-8.421, P = 0.001 for AML and HR = 2.718, 95% CI = 1.086-6.797, P = 0.03 for B-ALL). Our results indicated that overexpression of SLC38A1 was correlated with poor OS in both AML and B-ALL patients. Therefore, SLC38A1 may be used as a prognostic marker in acute leukemias. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s12288-025-02030-x.