Table 1 Association between clinicopathological factors and β-galactosidase (β-Gal) activity in hepatocellular carcinoma (HCC) tumour tissues.

From: Rapid fluorescence imaging of human hepatocellular carcinoma using the β-galactosidase-activatable fluorescence probe SPiDER-βGal

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)

  1. 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.
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