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Telomere changes in human hepatocellular carcinomas and hepatitis virus infected noncancerous livers
Author(s) -
Ohashi Kazuo,
Tsutsumi Masahiro,
Nakajima Yoshiyuki,
Kobitsu Kunihiko,
Nakano Hiroshige,
Konishi Yoichi
Publication year - 1996
Publication title -
cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.052
H-Index - 304
eISSN - 1097-0142
pISSN - 0008-543X
DOI - 10.1002/(sici)1097-0142(19960415)77:8<1747::aid-cncr50>3.0.co;2-w
Subject(s) - medicine , hepatocellular carcinoma , telomere , virology , virus , hepatitis a virus , pathology , hepatitis , hepatitis c virus , cancer research , dna , biology , genetics
BACKGROUND Telomeres, at the ends of eukaryotic chromosomes, are defined functionally as necessary for chromosome stability. Chromosome instability induced in part by loss of telomeric DNA has been considered to play a significant role in the development of human cancers. However, little is known about the status of telomeres per se during human hepatocellular carcinoma (HCC) development. METHODS This study was conducted to determine the length of terminal restriction fragments (TRFs) at the telomeric ends in 23 HCCs and 23 corresponding noncancerous liver tissues from the same patients harboring hepatitis virus infections, and in 5 samples of noncancerous livers without the hepatitis virus. The latter samples had been obtained as controls at surgery for metastatic liver tumors. RESULTS All 23 HCCs demonstrated reduction in TRF length compared with the corresponding noncancerous liver tissues with viral infection. The TRF in the latter cases also demonstrated a significant shortening as compared with the virus free control tissue, the degree being calculated to represent an average of 42 cell divisions. Reduction in TRF length in HCC samples tended to increase with the tumor diameter, although this failed to show statistical significance. CONCLUSIONS These results indicate that telomere shortening occurs during HCC development. The fact that this change is already evident in noncancerous liver tissues from patients with viral hepatitis suggests that it may play an important role in the associated generation of tumors. Cancer 1996;77:1747‐51.