Table 1.
Association between clinicopathological factors and β-galactosidase (β-Gal) activity in hepatocellular carcinoma (HCC) tumour tissues.
| Variable | n | β-galactosidase of tumour median (range) | p-Value | |
|---|---|---|---|---|
| Sex | Male | 58 | 0.214 (0.070–0.667) | 0.534 |
| Female | 10 | 0.262 (0.126–0.612) | ||
| Age | < 70 | 32 | 0.285(0.0702–0.67) | 0.194 |
| ≥ 70 | 36 | 0.208 (0.102–0.612) | ||
| BMI | < 22 | 24 | 0.198 (0.070–0.612) | 0.266 |
| ≥ 22 | 44 | 0.284 (0.102–0.667) | ||
| Maximum tumor size | < 25 mm | 34 | 0.207 (0.070–0.416) | 0.261 |
| ≥ 25 mm | 34 | 0.317 (0.103–0.667) | ||
| Differentitation | Well differentiated | 24 | 0.214 (0.102–0.667) | 0.532 |
| Moderately, poorly differentiated | 44 | 0.249 (0.070–0.612) | ||
| Background liver | NL, LC | 26 | 0.202 (0.070–0.574) | 0.294 |
| CH/LF | 42 | 0.313 (0.102–0.667) | ||
| Hepatitis virus | HBV, HCV | 27 | 0.206 (0.070–0.612) | 0.049 |
| Non-B, Non-C | 41 | 0.321 (0.103–0.667) | ||
| AFP | < 10 ng/mL | 45 | 0.199 (0.070–0.605) | 0.239 |
| ≥ 10 ng/mL | 19 | 0.313 (0.103–0.667) | ||
| PIVKAII | < 40 mAU/mL | 32 | 0.207 (0.070–0.667) | 0.360 |
| ≥ 40 mAU/mL | 32 | 0.309 (0.123–0.612) | ||
| ICG | < 15% | 37 | 0.213 (0.070–0.667) | 0.526 |
| ≥ 15% | 29 | 0.215 (0.102–0.504) | ||
| Liver damage | A | 65 | 0.213 (0.070–0.667) | 0.550 |
| B, C | 3 | 0.280 (0.185–0.371) | ||
β-Gal activity in HCC tumour tissues was analysed in relation to clinicopathological factors. β-Gal activity in the tumour tissue of patients not infected with hepatitis B virus (HBV) and hepatitis C virus (HCV) was significantly higher than that in the tumour tissue of patients infected with HBV and HCV. On analysing other clinicopathological factors (sex, age, BMI, background liver, AFP, PIVKAII, ICG, and grade of liver damage), β-Gal activity in the tumour tissues was not significantly different. A two-tailed Mann–Whitney U-test was used to analyse data. BMI; body mass index, NL; normal liver, CH; chronic hepatitis, LF; liver fibrosis, LC; liver cirrhosis, Non-B; patients not infected with HBV, Non-C; patients not infected with HCV, AFP; alpha-fetoprotein, PIVKAII; protein induced by vitamin K absence or antagonist-II, ICG; indocyanine green. Liver damage was defined based on the General Rules for the Clinical and Pathological Study of Primary Liver Cancer, Edition 6, Revised Version35.