A 43-year-old male was admitted to Seoul St. Mary's Hospital in January 2006. He had been a known hepatitis B carrier for 18 years, and abdominal sonography performed at the outpatient clinic incidentally revealed a mass in the right liver lobe. He had no history of diabetes or hypertension. Pertinent laboratory findings showed the following: a leukocyte count of 8,340/µL, hemoglobin concentration of 14.6 g/dL, platelet count of 251,000/µL, prothrombin activity time of 85%, aspartate aminotransferase of 38 IU/L, alanine aminotransferase of 62 IU/L, alkaline phosphatase of 180 IU/L, total bilirubin of 0.68 mg/dL, total protein concentration of 7.3 g/dL, and an albumin concentration of 3.05 g/dL. Serological tests performed on the patient to test for the hepatitis B "s" and "e" antigens were positive. Furthermore, the serum alpha-fetoprotein (AFP) concentration was 8.04 ng/mL. CT revealed a diffuse infiltrative HCC involving the right hepatic lobe with tumor thrombosis involving the right portal vein and the proximal portion of the left portal vein (Fig. 1A and 1B). HT treatment was targeted at the site of the portal vein thrombosis. The patient was immobilized with a whole-body vacuum, low-pressure foil (Body Fix System, Medical Intelligence, Schwabmuenchen, Germany) to minimize respiratory motion of the tumor and internal organs. A daily dose of 5 Gy was administered, at five fractions per week, to deliver a total dose of 50 Gy (Fig. 2). We performed CT scans at 2 (Fig. 1C and 1D) and 6 months (Fig. 1E and 1F) after treatment, which showed markedly improved portal vein thrombosis. After HT treatment, an intra-arterial chemoport was inserted at the hepatic artery 1 month later, and the patient received four cycles of chemotherapy with a monthly regimen of cisplatin (60 mg/m²), epirubicin (50 mg/m²), and 5-fluorouracil (200 mg/m²). One year after receiving HT, a 2-cm arterial enhancing nodule was discovered on the hepatic dome of the liver. The patient subsequently received successful radiofrequency ablation (RFA) for the enhancing nodule. He is currently alive and has been in good health for 23 months with subsequent successful treatments after the HCC diagnosis.

A 42-year-old female patient with HCC visited Seoul St. Mary's Hospital in January 2006. She was diagnosed with HCC in 2001 and had received a right hepatectomy at another hospital. Three years after the surgery (August 2004), she visited our hospital, and a lung metastasis was discovered. She received six intermittent cycles of chemotherapy from 2004 to 2005. After the six cycles of chemotherapy, she refused to visit the hospital. The laboratory findings upon admission showed the following: a leukocyte count of 2,500/µL, hemoglobin concentration of 11.5 g/dL, platelet count of 50,000/µL, prothrombin time activity of 78%, aspartate aminotransferase of 36 IU/L, alanine aminotransferase of 31 IU/L, alkaline phosphatase of 94 IU/L, total bilirubin of 0.65 mg/dL, total protein of 6.8 g/dL, and an albumin concentration of 3.86 g/dL. Additionally, serum AFP was 926.3 ng/mL. We performed chest X-rays upon admission, which showed an increase in the size of the metastatic lung lesions compared with her previous chest X-rays from 11 months earlier (Fig. 3A). The chest CT also showed an increase in the size of multiple metastatic lung lesions, but no increase in number (Fig. 3D). A CT of the abdomen also revealed an interval increase in the size of the HCC in the hepatic dome, compared with the abdominal CT from 1 year earlier. The patient received HT for her multiple lung lesions, with a daily regimen of 3-5 Gy, at five fractions per week, for a total dose of 30-50 Gy to each metastatic lung lesion (Fig. 4). A chest X-ray was performed at 2 and 6 months after the HT and revealed a marked decrease in the size of the multiple lung nodules (Fig. 3B and 3C). A chest CT similarly showed a vast decrease in the size of the lung nodules (Fig. 3E and 3F). Serum AFP 2 months after HT was 224.1 ng/mL. The patient received systemic chemotherapy treatment on a monthly regimen. Six months after receiving HT, a brain CT showed newly developed brain metastases. She received HT again for her multiple brain lesions, according to the same treatment protocol for her metastatic lung lesions (data not shown). A brain CT was performed at 3 months after the HT and revealed a marked decrease in the size of the multiple brain masses. She was alive 16 months after the initial HT for multiple metastatic lung tumors and died 6 months after receiving brain HT due to bleeding from a newly developed metastatic brain tumor.