Table 2.
Study Sample | Main Findings | Prognosis 1 | Reference |
---|---|---|---|
168 HCCs with viral and non-viral etiology | AKR1B10 overexpression associated with lower pT-classification Loss of AKR1B10 correlated with increased proliferative activity Poorer prognosis in patients with AKR1B10-negative HCCs compared with patients with AKR1B10- positive HCCs |
Favorable | [24] |
48 HCC with hepatitis C virus (HCV) | ≥6% up-regulation of AKR1B10 associated with ≥21-fold relative risk of HCC | Poor | [34] |
255 HCCs with viral and non-viral etiology | High AKR1B10 expression independently predicted longer RFS 2 and longer disease-specific survival. | Favorable | [32] |
109 HCCs with viral and non-viral etiology | AKR1B10 expression associated with free surgical margins, early BCLC 3 staging, and lack of metastasis Higher AKR1B10 expression associated with better OS 4, progression-free survival, and lower metastatic risk |
Favorable | [28] |
26 HCC with viral and non-viral etiology | Lower AKR1B10 expression was associated with worse RFS and OS. | Favorable | [30] |
43 HCC with HCV | High AKR1B10 expression independently predicted HCC. 5-year cumulative incidences of HCC were 22.8% and 2.2% in patients with high and low AKR1B10 expression, respectively. |
Poor | [35] |
8 HCC with HCV | High AKR1B10 expression was the only independent risk factor for HCC. 5-year cumulative incidences of HCC were 13.7% and 0.5% in patients with high and low AKR1B10 expression, respectively. |
Poor | [36] |
13 HCC with HBV | High AKR1B10 expression independently predicted HCC. 5-year cumulative incidences of HCC were 20.6% and 2.6% in patients with high and low AKR1B10 expression, respectively. |
Poor | [38] |
110 HCC with HBV | Higher AKR1B10 expression associated with higher DFS 5 and OS and low risk of early HCC recurrence | Favorable | [31] |
1 Based on high AKR1B10 levels; 2 RFS: recurrence-free survival; 3 BCLC: Barcelona Clinic Liver Cancer; 4 OS: overall survival; 5 DFS: disease-free survival.