The poor prognosis of hepatocellular carcinoma (HCC) was partly a result of the majority of unresectable HCCs in clinical patients. Fortunately, with the progress of regional cencer therapics and multimo-dality trealent, some of the licalized unresectable HCCs were converted to resectable ones. During the period 1960-1994, 72 of the 663 patients with surgically verified unresectable HCCs have been converted to resectable ones. During the period 1960-1994, 72 of the 663 patients with surgically verified unreseetable HCCs have been converted to rescctable. Sucessful cytoreduction with median diameter reduced from 10 cm to 5 cm was mainly a result of the triple or double combination treatment with hepatic artery ligation, hepatic artery cannulation with infusion, radioimmunotherapy. and fractionated regional radiotherapy. The interval hetween the first operation and the sequential reection was 5 months. The operative mortality was 1.4% for sequential resection, and the 5-year sursival was 62.1%. Analysis of factors influencing sequenlial resection rate revealed HCCs that were single nodule, well encapsulated, situated at right lobe or hepatic hilum, associated with micromodular cirrhosis, and treated with triple or double combination modalities had higher sequential resection rate as compared to their counterparts. Analysis of factors influencing sursival after sequential resection revealed that HCCs with a solitary lumor confined in one lobe, without tumor embolus, and without residual cancer in specimen of sequential resection, had longer survival. It is suggesled that localized unreseelable, solitary, well encapsulated, reght lobe or hilar HCC, associated with micronodular cirrhosis, will be good candidates for cytoreduction and sequential resection; and HCCs with unilateral involvement, without tumor embolus, and with complete necrosis of tumor after multimodality trcatment favored better prognosis.

To understand the genetic mechanisms underlying the progression of hepatocellular carcinoma(HCC) metastasis, differences of genomic alter-ations between 10 pairs of primary HCC tumors and their matched metastatic lesions were analyzed by comparative genomic hybridization. Several chromosomal alterations including loss of 8p, 4q, 17p, and 19p, gain of 5p and high-level amplification of lq12-q22 were detected in two or more cases. The most significant finding is the loss of 8p which was detected in 8 metastatic tumors but only in 3 corresponding primary tumors(P=0.03). This result suggests that the deletion of chromosome 8p might contribute to the development of HCC metastasis. Another inter-esting result is the detection of a minimum high-lever amplification region at lq12-q22 in HCC. This result provides a candidate amplification region at lq12-q22 in HCC. This result provies a candidate amplification region in HCC for further study to identify amplified oncogenes related to the development or progression of HCC. Finally, this study provides a prac-ticable model to detect specific genetic alterations related to the tumormetastasis through comparing the primary tumor and its corresponding metastatic lesion using comparative genomic hybridization technique.