To elucidate cytogenetic alterations underlying human hepatocellular carcinomas (HCCs), we used a comparative genomic hybridization (CGH) method to analyze 41 cases of hepatocellular carcinoma (HCC) including 15 well differentiated HCCs, 14 moderately differentiated HCCs, and 12 poorly differentiated HCCs. Of these, 27 patients were chronically infected with hepatitis C virus (HCV), and the remaining patients were positive for hepatitis B virus (HBV). The most common sites of increase in DNA copy number were 1q (78% of the cases) and 8q (66%) with minimal overlapping regions at 1q24-25 and 8q24, respectively. Frequent decreases in copy number were observed at 17p (51%), 16q (46%), 13q13-14 (37%), 4q13-22 (32%), 8p (29%), and 10q (17%). In 6 cases (15%), an amplification was found in the region of 11q13. A gain of 8q24 was significantly associated with well-differentiated HCCs (PF.05), whereas a loss of 13q13-14 and amplification of 11q13 were linked to moderately and poorly differentiated HCCs (PF.01). These observations suggest that a gain of 8q24 is an early event and that a loss of 13q13-14 and amplification of 11q13 are a late event in the course of liver carcinogenesis. A gain of 10q (7/41) was detected exclusively in cases with HCV infection. In contrast, an amplification of 11q13 was preferentially found in HBV-positive HCCs. These findings raise the hypothesis that, although many genetic alterations are basically common to both HCV-positive and HBV-positive tumors, the process of carcinogenesis may be to some extent different between these two types of tumors. (HEPATOLOGY 1999;29:1858-1862.) Hepatocellular carcinoma (HCC) is one of the most common human malignant tumors in the world. 1 It is widely accepted that hepatitis B (HBV) or C virus (HCV) infection, subsequent chronic inflammation and hepatocyte regeneration play important roles in the development of HCC. 2,3,4 However, the effects of viral infection on hepatocellular transformation remain to be determined. Accordingly, it remains unknown whether carcinogenetic process is different in HBV-positive and HCV-positive livers. HCC, like many other tumors, is considered to develop and progress as a consequence of an accumulation of genetic alterations. 5 Many investigators have made varying attempts to find genes implicated in hepatocarcinogenesis to construct a genetic pathway in the progression of HCC. 6,7,8,9 Although frequent allelic losses at loci of chromosomes 1p, 4q, 5p, 5q, 8p, 10p, 11q, 13q, 16q, and 17p have been reported in HCCs, 10,11 most of these studies failed to provide consistent information concerning genetic changes leading to the evolution of HCC. Comprehensive analysis is necessary to thoroughly understand the complicated genetic alterations in malignant tumors. Determination of these comprehensive genetic changes in solid tumors is practically difficult, because the examination of many individual genes by conventional methods is laborious and cumbersome. Screening for chromosomal regions with frequent gains and losses is one of t...

BACKGROUNDThe therapeutic efficacy of radiofrequency ablation (RFA) for hepatocellular carcinoma (HCC) is limited by the small volume of coagulation necrosis obtained at each activation of the RF system and the sometimes irregular burn shape due to the proximity of large vessels that have a cooling effect. To improve the efficacy of RFA, the authors designed RFA with balloon occlusion of the hepatic artery (balloon‐occluded RFA). In this study, we investigated the efficacy of balloon‐occluded RFA and compared the coagulation diameters obtained with balloon‐occluded RFA and standard RFA.METHODSWe retrospectively studied 31 patients with 42 HCC lesions measuring less than 4 cm in the greatest dimension. We performed balloon‐occluded RFA for 12 patients (n = 15 nodules) and standard RFA for 19 patients (n = 27 nodules). Initial therapeutic efficacy was evaluated with dynamic computed tomography scan performed 2 weeks after one treatment.RESULTSThere were no significant differences in the ablation conditions such as the frequency of a fully expanded electrode, the number of needle insertions, application cycles, or treatment times between the two groups. However, the greatest dimension of the area coagulated by balloon‐occluded RFA was significantly larger (greatest long‐axis dimension, 36.6 ± 3.8 mm; greatest short‐axis dimension, 30.1 ± 6.0 mm; n = 15 lesions) than that coagulated by standard RFA (greatest long‐axis dimension, 26.7 ± 6.4 mm; greatest short‐axis dimension, 23.1 ± 5.0 mm; n = 27 lesions; greatest long‐axis dimension, P < 0.001; greatest short‐axis dimension, P < 0.001).CONCLUSIONSBalloon‐occluded RFA is superior to standard RFA for the treatment of many hepatocellular lesions, especially when larger volumes of coagulation are required. Cancer 2002;95:2353–60. © 2002 American Cancer Society.DOI 10.1002/cncr.10966

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Tumors arising from the liver, biliary tract and pancreas, which originate in the foregut and are in close anatomical proximity to each other, sometimes show similar histological features. No studies have focused on genetic similarities and differences between tumors of these organs. To elucidate the similarities and differences in DNA copy number alterations between tumors of these organs, we applied comparative genomic hybridization (CGH) to cancers of the liver (31 cases), biliary tract (42 cases) and pancreas (27 cases). Some alterations were common to tumors of all three organs, and some were preferential in certain types of tumor. Gains of 1q and 8q and losses of 8p and 17p were common to all tumors. In contrast, 13q14 and 16q losses were detected exclusively in hepatocellular carcinomas (HCCs; p < 0.01). The incidence of 17q21 gain and 5q loss was higher in biliary tract cancers than in the other two types (p < 0.05). Pancreatic cancers exhibited higher incidence of 5q14-q23 gain and 19p loss than tumors of other organs (p < 0.01). Gains of 7p, 7q, 12p and 20q and losses of 3p, 6q, 9p and 18q were frequent in both biliary tract and pancreatic cancers but rare in HCCs (p < 0.05). The present results suggest that although genes located at 1q, 8p, 8q and 17p are frequently involved in HCC, biliary tract and pancreatic cancer, at least some of the genes implicated in carcinogenesis are different between these three types. It is also suggested that CGH analysis is useful as a potential adjunct for the diagnosis and management of these tumors of organs that are anatomically close to one another.