Growth inhibition of experimental liver metastasis by portal embolization.

BACKGROUND/AIMS: The current available treatments for multiple liver cancer are not satisfactory. The aim of this study is to investigate the effects of portal embolization (PE) on the growth of experimental liver metastasis in rats. METHODOLOGY: One million of tumor cells (AH130 hepatoma cell originated from rat) were injected intraportally into Donryu rats to produce liver metastasis. The rats were divided into five groups as follows: Group A, laparotomy (as control); Group B, embolization of the left branch of portal vein; Group C, ligation of the left branch of the portal branch (PVL); Group D, ligation of the left branch of the hepatic artery (HAL); Group E, left hepatic resection (HR). Body weight, liver weight, weight ratio of the right lobes to the total liver, tumor occupation rates, liver tissue blood flow, liver dye-staining test, and immunohistochemical stainings were studied in each group. The survival duration of each group was also studied. RESULTS: Significantly hypertrophy of the right lobes and atrophy of the left lobes was observed in Group B and C, Body weight increased significantly in Group B and C compared with Group A, D, and E. The tumor occupation rates in the right lobes were significantly smaller in Group B and C than those in Group A, D, and E. Liver tissue blood flow of the left lobes changed from 31.9 +/- 6.5 ml/mn/100 g to 9.0 +/- 3.2 on clamping the main portal vein and to 18.2 +/- 4.2 on clamping the left portal branch, suggesting a compensatory increase of hepatic artery flow in the left lobes in Group B and C. PE resulted in marked hepatic hypertrophy and significant reduction of tumor growth in the non-embolized lobes. CONCLUSIONS: PE resulted in marked hepatic hypertrophy and significant reduction of tumor growth in the non-embolized lobes, probably owing to decrease in arterial flow in the non-embolized lobes. The attractive concept of PE may have utility in clinical setting in the event of multiple liver cancer.

Effect of follistatin on rat liver regeneration and tumor growth after portal occlusion.

BACKGROUND/AIMS: Although follistatin is known to be a positive regulator in liver regeneration after hepatectomy, the effects of follistatin on regeneration following portal occlusion and on tumor growth are not known. METHODOLOGY: In experiment 1, rats were injected with follistatin immediately following 70% hepatic resection (HR), ligation of the left portal vein (PVL), or ligation of the left hepatic artery (HAL). Hepatic regenerative activity then was determined. In experiment 2, rats were injected intraportally with AH130 tumor cells. At 7 days after injection, the same procedures were carried out as in experiment 1. In a third experiment, in vitro, AH130 cells were cultured with various concentrations of activin A or follistatin, and cell proliferation was assessed. RESULTS: In experiment 1, follistatin did not accelerate liver regeneration after PVL. In experiment 2, follistatin significantly increased liver weight after HR, but did not accelerate tumor growth in any group. In vitro, neither follistatin nor activin affected proliferation of tumor cells. CONCLUSIONS: The mechanism of liver regeneration after PVL appears to differ from that after HR. Follistatin acts as a growth promoter for hepatocytes, but not for cancer cells.