Telomere length in human liver diseases

Yoshiaki Urabe, Kazuhiro Nouso, Toshihiro Higashi, Harushige Nakatsukasa, Naoki Hino, Kouzou Ashida, Nobuyuki Kinugasa, Keigo Yoshida, Shuji Uematsu, Takao Tsuji

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49 Citations (Scopus)


To determine the role of telomere-mediated gene stability in hepatocarcinogenesis, we examined the telomere length human liver without chronic liver diseases and hepatocellular carcinomas (HCC). The mean telomere restriction fragment (TRF) length of normal liver (n = 13), chronic hepatitis (n = 11), liver cirrhosis (n = 24) and HCC (n = 24) was 7.8 ± 0.2, 7.1 ± 0.3, 6.4 ± 0.2 and 5.2 ± 0.2 kb, respectively (mean ± standard error). TRF length decreased with a progression of chronic liver diseases and that in HCC was significantly shorter than that in other chronic liver diseases (p < 0.05). The ratios of TRF length of HCC to that of corresponding surrounding liver of well differentiated (n = 7), moderately differentiated (n = 10) and poorly differentiated (n = 4) HCCs were 0.83 ± 0.06, 0.75 ± 0.05 and 0.98 ± 0.09, respectively. The ratio of poorly differentiated HCC was significantly higher than that of moderately differentiated HCC (p < 0.05). A comparison between the size and telomere length ratio of moderately differentiated HCCs revealed a decrease of the ratio with size until it reached 50 mm in diameter. In contrast, the ratio increased as the size enlarged over 50 mm. These findings suggest that the gene stability of the liver cells mediated by the telomere is reduced as chronic liver disease progresses and that telomerase is activated in poorly differentiated HCC and moderately differentiated HCC over 50 mm in diameter.

Original languageEnglish
Pages (from-to)293-297
Number of pages5
Issue number5
Publication statusPublished - Oct 1996


  • Carcinoma
  • Hepatocarcinogenesis
  • Hepatocellular
  • Telomere

ASJC Scopus subject areas

  • Hepatology


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