Article Figures & Data
Figures
- Figure 1.
The presence of a single functional compound of KIR-HLA genotype did not affect HCC recurrence. The effect of each compound genotype (KIR2DL1-C2, KIR2DL2-C1, KIR3DL1-BW4, KIR3DL2-A3/11) on HCC recurrence was analyzed by propensity score–matched studies using nine variables (age, sex, etiology, tumor number, maximum diameter, histologic differentiation, vascular invasion, satellite lesion, and surgical margin). The 5-year cumulative risk of recurrence was compared between one-to-two or two-to-one patient pairs with or without each compound KIR-HLA genotype. A, KIR2DL1-C2; B, KIR2DL2-C1; C, KIR3DL1-Bw4; and D, KIR3DL2-A3/11.
- Figure 2.
The multiplicity of compound KIR-HLA genotypes stratified the recurrence risk of HCC. Kaplan–Meier analyses of the 5-year cumulative risk of recurrence (A) and OS (B) for 170 patients were performed according to the number of functional compound KIR-HLA genotypes. Propensity score–matched analyses of the 5-year cumulative risk of recurrence (C) and OS (D) were also performed for patients with at least three compound genotypes (highly licensed NK group) and patients with one or two compound genotypes (poorly licensed NK group). The cumulative risk of recurrence in the highly licensed NK group was significantly lower than in the poorly licensed NK group. aHR, adjusted HR.
- Figure 3.
The lower cumulative risk of recurrence in the highly licensed NK group was significant among the non–HCV-related cohort. A, according to the presence or absence of HCV infection, Kaplan–Meier analyses of the 5-year cumulative risk of recurrence were performed for 138 matched patients belonging to the highly and poorly licensed NK groups. Further subgroup analyses were performed in non–HCV-related patients (B) and HCV-related patients (C).
Tables
- Table 1.
Cumulative risk of recurrence and overall survival of patients with HCC according to clinicopathologic characteristics and compound KIR-HLA genotypes
Total patients (N = 170) HCV-related patients (n = 97) Cumulative risk of recurrence OS Cumulative risk of recurrence OS P HR (95% CI) P HR (95% CI) P HR (95% CI) P HR (95% CI) Age (≤65 vs. >65 years) 0.745 NA 0.362 NA 0.626 NA 0.592 NA Sex (male vs. female) 0.078 1.54 (0.99–2.53) 0.966 NA 0.554 NA 0.216 NA Etiology (HBV vs. HCV vs. others) 0.448 NA 0.117 NA NA NA NA NA Tumor number (≥2 vs. 1) 0.010 1.57 (1.06–2.31) 0.039 1.64 (1.11– 2.39) 0.088 1.56 (0.92–2.51) 0.604 NA Maximum diameter (≤50 mm vs. >50 mm) 0.222 NA 0.511 NA 0.749 NA 0.313 NA Histologic differentiation (G1+G2 vs. G3) 0.253 NA 0.498 NA 0.866 NA 0.909 NA Vascular invasion 0.733 NA 0.851 NA 0.612 NA 0.454 NA Satellite lesion 0.657 NA 0.743 NA 0.451 NA 0.486 NA Surgical margin (<5 mm vs. ≥5 mm) 0.126 NA 0.162 NA 0.039 1.88 (0.98–3.36) 0.003 1.88 (0.97 – 3.37) KIR2DL1-C2 0.113 NA 0.754 NA 0.189 NA 0.964 NA KIR2DL2-C1 0.253 NA 0.945 NA 0.456 NA 0.745 NA KIR2DL3-C1 0.793 NA 0.283 NA 0.694 NA 0.105 NA KIR3DL1-Bw4 0.269 NA 0.359 NA 0.572 NA 0.935 NA KIR3DL2-A3/11 0.585 NA 0.570 NA 0.845 NA 0.986 NA Number of KIR-HLA genotypes (≥3 vs. ≤2) 0.016 0.61 (0.38–0.94) 0.224 NA 0.130 NA 0.735 NA NOTE: Cumulative risk of recurrence and OS were compared by log-rank statistics for univariate analysis. Cox proportional hazards model was conducted for multivariate survival analysis. Only variables presenting P < 0.1 in the univariate analysis were included in the multivariate model. P < 0.05 was considered statistically significant.
Abbreviation: NA, not assessed.
Supplementary Table S1
Files in this Data Supplement:
- Data Supplement - One hundred seventy HCC patients who underwent curative hepatectomy were enrolled based on the following inclusion criteria: presence of histologically confirmed HCC; preserved preoperative liver function (Child-Pugh grade A); no residual tumor after surgery; and no evidence of comorbid malignant tumor. Background characteristics and prognoses of the patients and tumors are summarized.
- Data Supplement - KIR and HLA genotyping was performed using the reverse SSP-PCR method. Presence of the HLA ligand for KIR was determined according to the HLA genotypes.
- Data Supplement - Background characteristics of patients before and after propensity score matching for each functional compound KIR-HLA genotype are summarized.
- Data Supplement - The effect of each compound genotype (KIR2DL1-C2, KIR2DL2-C1, KIR3DL1-BW4, and KIR3DL2-A3/11) on 5-year OS was analyzed by propensity score-matched studies using nine variables (age, sex, etiology, tumor number, maximum diameter, histological differentiation, vascular invasion, satellite lesion, and surgical margin). The 5-year OS was compared between one-to-two or two-to-one patient pairs with or without each compound KIR-HLA genotype. (A) KIR2DL1-C2; (B) KIR2DL2-C1; (C) KIR3DL1-Bw4; and (D) KIR3DL2-A3/11.
- Data Supplement - Propensity score matching was performed using nine variables (age, sex, etiology, tumor number, maximum diameter, histological differentiation, vascular invasion, satellite lesion, and surgical margin) for patients with at least three compound genotypes (highly licensed NK group) and patients with one or two compound genotypes (poorly licensed NK group). Background characteristics before and after matching are summarized.
- Data Supplement - (A) According to TNM stages, Kaplan-Meier analyses of the 5-year cumulative recurrence risk were performed for the 138 matched patients belonging to the highly and poorly licensed NK groups. Further subgroup analyses were performed for patients with (B) stage I, (C) stage II, and (D) stage IIIA HCC.
- Data Supplement - Cumulative risk of recurrence and overall survival were compared by log-rank test for univariate analyses. The Cox proportional hazards regression model was performed for multivariate survival analysis. Only variables yielding P < 0.1 in the univariate analysis were included in the multivariate model.
Volume 2, Issue 12
