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Letter to the Editor |
Department of Surgery II, Kyushu University, Faculty of Medicine, Fukuoka 812 Japan; Department of Food Science and Technology, Kyushu University, Faculty of Agriculture, Fukuoka 812, Japan; Department of Pathology II, Faculty of Medicine, Fukuoka 812, Japan
ABSTRACT
Recently, Kondo et al. (1) reported that the level of COX1 -2 increased from normal liver to chronic hepatitis to cirrhosis. An increase in COX-2 expression in the nontumor tissues was significantly associated with relapse of HCC, which is of great interest from a clinical point of view. They suggested that the presence of active inflammation, which was highly correlated with COX-2 expression, was involved in the development of tumor relapse. On the other hand, a significant association was observed between COX-2 expression and the histological grade of HCC. Well- and moderately differentiated HCCs expressed COX-2 more strongly than poorly differentiated HCC. Taken together, these findings indicate that COX-2 may be associated with the early process of the progression of HCCs. COX-2 is a rate-limiting enzyme in the conversion of AA to prostaglandins (PGs) and other eicosanoids. AA is largely derived by biotransformation from an essential fatty acid, LA. Therefore, such a sharp fluctuation in the COX-2 enzyme activity (1) might affect the hepatic tissue fatty acid composition, especially the amounts of AA and LA. We recently determined the fatty acid composition of both HCC and nontumor tissues that had been surgically resected in the Department of Surgery II, Kyushu University. Eighteen HCC specimens with adjacent nontumor tissue, involving 10 cases of chronic viral hepatitis and 8 cases of cirrhosis, and 8 surgically resected, histologically normal liver tissue were used. Each HCC was histologically graded into one of three categories: well differentiated, moderately differentiated, and poorly differentiated, according to the criteria proposed by the Liver Cancer Study Group of Japan (2) . The hepatic tissue specimens were extracted according to the method of Folch et al. (3) . The tissue fatty acids were converted to methyl esters and analyzed by gas chromatography on a SUPELCOWAX-10 fused silica capillary column (30-m x 0.53-mm x 1.0-µm film thickness).
The content of both the LA and the AA (Fig. 1, A and B
, respectively) varied in a manner quite
similar to that of COX-2 expression (1)
. The lowest amount
of AA was detected in the normal liver, and the amount of AA increased
from normal liver to chronic hepatitis to cirrhosis (Fig. 1
B). These findings reinforce the suggestion that the amount
of AA may also be associated with the early stages of hepatic
carcinogenesis. On the other hand, well-differentiated HCC contained
the highest LA content among the three histological grades of HCC, and
the amount of LA content decreased when the HCC was graded more poorly
differentiated (Fig. 1
A). This is the first
demonstration that the tumor dedifferentiation of human HCC is
correlated with the tissue fatty acid composition.
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FOOTNOTES
1 The abbreviations used are: COX, cyclooxygenase;
HCC, hepatocellular carcinoma; AA, arachidonic acid; LA, linolenic
acid; PUFA, polyunsaturated fatty acid. 
2 To whom requests for reprints should be
addressed, at The Department of Surgery, Medical Institute of
Bioregulation, Kyushu University, Beppu 874-0838, Japan. Phone:
81-977-27-1650; Fax: 81-977-27-1651; E-mail: tohru{at}tsurumi.beppu.kyushu-u.ac.jp
Received 4/18/00; revised 9/ 6/00; accepted 9/ 6/00.
REFERENCES
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