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Keywords:

  • hepatocellular carcinoma -transcatheter arterial chemoembolization -Bcl-2 - vascular endothelial growth factor -anoxia

Abstract: Aims/Background: Transcatheter arterial chemoembolization (TAE) of hepatocellular carcinoma (HCC) causes anoxia. Escape of cancer cells from anoxic injury may be enhanced by induction of proteins which provide resistance to apoptosis. Methods: We examined HCCs immuno-histochemically for Bcl-2, vascular endothelial growth factor (VEGF), p53, and Ki67. The staining intensity for VEGF, a protein induced by anoxia, was assessed morphometrically with a computer-assisted image-analyzer. Results: The frequency of Bcl-2 positive cells was higher in HCCs that had undergone TAE (TAE HCC) than that in HCCs that had not undergone TAE (41.75 ± 15.06 vs. 1.01 ± 0.79 cells/1000 cells, p=0.0173). The frequency of p53- or Ki67-positive cells was not increased after TAE. Of 12 TAE HCCs, 7 had Bcl-2 positive HCC cells and 6 had clusters of Bcl-2 positive cells. In contrast, 2 of 11 HCCs that had not undergone TAE had only a few, sporadically distributed, Bcl-2-positive cells. The staining intensity for VEGF was higher in Bcl-2 positive than in Bcl-2 negative areas (1.208 ± 0.091 vs. 1.071 ± 0.017, p=0.0222). Furthermore, the VEGF staining intensity in Bcl-2 positive areas of TAE HCCs was higher than in Bcl-2 negative areas (1.296 ± 0.126 vs. 1.066 ± 0.024, p= 0.0186), while in HCCs that had not undergone TAE the staining intensity was similar. Conclusions: TAE of HCC can induce Bcl-2 expression, possibly through anoxic stress.