Cell proliferation and cell loss in nodule-in-nodule hepatocellular carcinoma

Hepatogastroenterology. 1999 Mar-Apr;46(26):813-9.

Abstract

Background/aims: In order to clarify the significance of the balance between cell proliferation and cell loss during the progression of hepatocellular carcinoma, 16 operative specimens of nodule-in-nodule hepatocellular carcinoma were investigated.

Methodology: In 16 specimens, cell proliferation was evaluated by the expression of Ki-67 nuclear antigen, and cell loss was also examined by the method of terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL). The expressions of p53 protein, bcl-2 protein and Fas antigen were also investigated to clarify the relationship between their expression and cell kinetics.

Results: The Ki-67 labeling index of the inner nodules was higher than that for the outer nodules (18.9% vs. 7.2%; p < 0.05) and the TUNEL labeling index of the inner nodules was also higher than that for the outer nodules (12.8% vs. 6.6%; p < 0.05). The increasing rate of the Ki-67 labeling index from Edmondson's grade I to II was 3.9 +/- 3.0, that from grade II to III was 3.9 +/- 2.4, while the increasing rate of the TUNEL labeling index from grade I to II was 2.7 +/- 0.3 and that from grade II to III was 1.7 +/- 0.2 (p < 0.05). p53 Protein was observed in 5 cases, while bcl-2 protein was found in 4 cases in the border area of the inner nodule. However, Fas antigen was found in none of the examined cases. Regarding the Ki-67 positive rate in the inner nodule, the Ki-67 positive rate in the p53 protein positive cases was significantly higher than that in the negative cases (30.3 +/- 15.4 vs. 11.9 +/- 9.2; p < 0.05). However, the TUNEL labeling index was not affected by the expression of those proteins.

Conclusions: This study suggested that tumor progression depends on a disturbance in the cell kinetic balance caused not by a decrease in the absolute amount of cell loss but in the chaotic balance between cell loss and cell proliferation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis / physiology*
  • Carcinoma, Hepatocellular / pathology*
  • Cell Division / physiology*
  • Humans
  • Immunoenzyme Techniques
  • In Situ Nick-End Labeling
  • Ki-67 Antigen / analysis
  • Liver / pathology
  • Liver Neoplasms / pathology*
  • Mitotic Index
  • Prognosis
  • Proto-Oncogene Proteins c-bcl-2 / analysis
  • Tumor Suppressor Protein p53 / analysis
  • fas Receptor / analysis

Substances

  • Ki-67 Antigen
  • Proto-Oncogene Proteins c-bcl-2
  • Tumor Suppressor Protein p53
  • fas Receptor