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Summary We performed an experimental study on slow releasing anticancer drug implantation treatment as a new therapy for hepatocellular carcinoma. Hydroxyapatite (HAP) was chosen for the carrier material and doxorubicin hydrochloride (DOX) for anticancer agent. DOX-HAP was produced by adsorbing DOX to porous HAP particles of 1375 ± 125 gm diameter using the freeze drying method. In vitro experiments showed slow release of the drug resulting in the steady release of DOX from HAP for I month duration. In healthy white rabbits with DOX-HAP implantation in the liver, serum DOX was not detectable, and DOX release rate was stable at the implanted region after 7, 14, and 21 days. When DOX-HAP (DOX; 100mg kg-') was administered to mice with sarcoma 180, an improved survival rate was observed without acute toxicity.We also found that VX2 liver tumour growth on white rabbit was inhibited by implantation of DOX-HAP, without acute toxicity. We hope that DOX-HAP implantation therapy will open up new avenues for the treatment of hepatoma.

The effect of biliary endoprosthesis was evaluated in 13 patients with major bile duct obstruction secondary to invasion by hepatocellular carcinoma. In 12 patients major portal vein branches were also invaded by the tumors. After several days' instillation of nasobiliary or percutaneous drainage tubes to flush the bile ducts, biliary endoprosthesis was performed either endoscopically (N = 9) or percutaneously (N = 4). Significant decrease (less than 50% of initial values) of alkaline phosphatase and bilirubin levels was observed in eight and two patients on day 20, respectively. Twelve patients died of hepatic failure at 27-132 days (mean 60 days). One patient without portal vein involvement is currently alive at 300 days. Biliary endoprosthesis has a limited role in the palliation of bile duct obstruction secondary to hepatocellular carcinoma, and the prognosis may be influenced mainly by the underlying hepatic function.

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The progressive expansion of calcification into the wall of the stomach and peritoneal metastatic foci was observed in a 31-year-old female with Borrmann type 4 calcified advanced gastric cancer. Despite treatment with systemic lentinan, uracil tegaful and mitomycin C, together with intraperitoneal injections of mitomycin C, OK-432 and prednisolone, the patient died 27 months after first presentation. The case provided a useful means of studying the mechanism of calcification.