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Frequent loss of heterozygosity on chromosome 22 in hepatocellular carcinoma

✍ Scribed by Kazuhiro Takahashi; Jiro Kudo; Hiromi Ishibashi; Yasuhiko Hirata; Yoshiyuki Niho

Publisher: John Wiley and Sons
Year: 1993
Tongue: English
Weight: 665 KB
Volume: 17
Category: Article
ISSN: 0270-9139
DOI: 10.1002/hep.1840170508

No coin nor oath required. For personal study only.

✦ Synopsis

We investigated 24 hepatocellular carcinomas in Japan to find loss of heterozygosity with 15 polymorphic DNA markers that detect allelic losses at specific chromosome loci. Loss of heterozygosity on chromosomes lOq, 17p and 22q was detected in 3 of 12 (26%), 9 of 21 (43%) and 5 of 15 (33%) informative cases of hepatocellular carcinoma, respectively. This is the first report of loss of heterozygosity on chromosome 22q in hepatocellular carcinoma; the newly recognized common chromosome loss was considered to exist between D22S9 and D22SlO on 22q11. On the basis of this and other studies, we believe it is likely that such a chromosome loss in hepatocellular carcinoma is a signal for malignant transformation and that loss of unknown genes on chromosomes lOq, 17p and 22q may contribute to tumor progression in hepatocellular carcinoma. (HEPATOLOGY 1993; 17:794-799.)

Liver cancer is the third most common cause of cancer death, following gastric and lung cancer, in Japan, afflicting 16.5 of 100,000 Japanese in 1985 (1). In Japan, approximately 90% of liver cancer is HCC, which is known to have a strong association with chronic hepatitis B or hepatitis C virus infection (2, 3). More than 80% of HCC cases are clinically preceded by cirrhosis (4). Pathological investigations have revealed the occurrence of well-differentiated HCC from adenomatous hyperplasia, which is usually followed by progression to the increased size of poorly differentiated HCC and, finally, by dissemination as intrahepatic or extrahepatic metastasis by way of the portal or hepatic veins (5,6). These serial changes in the progression of HCC lead to speculation that HCCs involve multiple genetic alterations, which have been well investigated in colorectal cancers (7).

Recent studies have demonstrated that allelic losses from chromosomes l p (8), 4q (9-ll), 5q (12, 13), 1Oq

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