Carcinogenesis, Vol 19, 1103-1107, Copyright © 1998 by Oxford University Press
M Yoshie, H Nishimori, GH Lee and K Ogawa
When hepatocytes isolated from mouse liver are cultivated in vitro, a small
fraction of cells can survive, forming colonies, while most cells die
within a few weeks. We compared the colony forming capacity of hepatocytes
in three mouse strains; two strains susceptible for hepatocarcinogenesis,
C3H/HeJ (C3) and DBA/2J mice (D2), and one resistant strain, C57BL/6J mice
(B6). The colony forming capacity was about 3:2:1 for D2, C3 and B6 at the
4th week after start of culture, indicating that this capacity correlated
with the susceptibility to tumor induction. When the colony forming
capacity was compared in F1 hybrids between the three strains, the high
colony forming capacity was dominant, again resembling the trait for
hepatocarcinogenesis. In F1 hybrids between the two susceptible strains,
the colony numbers were more than those of the parental strains, indicating
the high colony forming capacity of the two susceptible strains to be
additive. During 4 weeks of culture period, the cells continuously
proliferated, but fairly large numbers of cells died, some showing
characteristics of apoptosis and others of lysis. Although the
proliferation rate was not different among the three strains until the 2
week time point, it was significantly lower in B6 than in C3 or D2 strains
by the 4th week. On the other hand, the cell death rate was lower in D2
cells than in B6 or C3 cells after 2 weeks. These results indicate that the
genetic background affects proliferation and death rates of cultured
hepatocytes, which may be related to the different colony forming capacity
of these three strains.
ARTICLES
High colony forming capacity of primary cultured hepatocytes as a dominant trait in hepatocarcinogenesis-susceptible and resistant mouse strains
Department of Pathology, Asahikawa Medical College, Nishikagura, Japan.
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  H. Tanaka, M. Yamamoto, N. Hashimoto, M. Miyakoshi, S. Tamakawa, M. Yoshie, Y. Tokusashi, K. Yokoyama, Y. Yaginuma, and K. Ogawa Hypoxia-Independent Overexpression of Hypoxia-Inducible Factor 1{alpha} as an Early Change in Mouse Hepatocarcinogenesis Cancer Res., December 1, 2006; 66(23): 11263 - 11270. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S.-i. Ueda, Y. Basaki, M. Yoshie, K. Ogawa, S. Sakisaka, M. Kuwano, and M. Ono PTEN/Akt Signaling through Epidermal Growth Factor Receptor Is Prerequisite for Angiogenesis by Hepatocellular Carcinoma Cells That Is Susceptible to Inhibition by Gefitinib. Cancer Res., May 15, 2006; 66(10): 5346 - 5353. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K Iida, C J Rosen, C Ackert-Bicknell, and M O Thorner Genetic differences in the IGF-I gene among inbred strains of mice with different serum IGF-I levels J. Endocrinol., September 1, 2005; 186(3): 481 - 489. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Ishizaki, M. Yoshie, Y. Yaginuma, T. Tanaka, and K. Ogawa Loss of Igf2 Imprinting in Monoclonal Mouse Hepatic Tumor Cells Is Not Associated with Abnormal Methylation Patterns for the H19, Igf2, and Kvlqt1 Differentially Methylated Regions J. Biol. Chem., February 14, 2003; 278(8): 6222 - 6228. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Ogawa, M. Osanai, M. Obata, K. Ishizaki, and K. Kamiya Gain of chromosomes 15 and 19 is frequent in both mouse hepatocellular carcinoma cell lines and primary tumors, but loss of chromosomes 4 and 12 is detected only in the cell lines Carcinogenesis, November 1, 1999; 20(11): 2083 - 2088. [Abstract] [Full Text] [PDF]
|
|