-transparent.png){kind=logo}
The process of chemical hepatocarcinogenesis is characterized by the appearance of preneoplastic lesions showing changes in the expression of various marker enzymes. We have analyzed the phenotype of small preneoplastic foci and expansively growing nodules in liver sections obtained from rats treated with various carcinogens. Changes within the lesions in canalicular adenosine triphosphatase, gamma-glutamyl transpeptidase, NADPH-(cytochrome P-450) reductase, cytochrome P-450 PB2, epoxide hydrolase, and glycogen content were detected by means of enzyme histochemical and immunohistochemical staining procedures. In parallel sections the expression of albumin messenger RNA was investigated by in situ hybridization using a 35S-labeled albumin specific complementary DNA probe. In general, small preneoplastic lesions showed unchanged levels of albumin messenger RNA. In contrast, the expression of albumin messenger RNA was found to be reduced to varying degrees in large hepatic nodules. An expression of alpha-fetoprotein messenger RNA could not be detected in any of the nodules. No direct correlation between the enzyme phenotype of the lesions and the degree in reduction of albumin messenger RNA could be established except that the reduction was most pronounced in nodules which had lost their ability to store glycogen. Since the synthesis and excretion of albumin is a typical function of the differentiated hepatocyte in the adult animal, the observed decrease in albumin messenger RNA expression in large hepatic nodules is in accordance with the hypothesis of a gradual dedifferentiation or retrodifferentiation of the cell population during carcinogenesis. Hyperplastic nodules produced by continuous treatment of rats with 4-dimethylaminoazobenzene showed increased rather than decreased albumin levels. The analysis of albumin messenger RNA expression might therefore be used as a tool to discriminate between nodules of differing biological nature and fate.
M Schwarz, and
G Peres, and
D G Beer, and
M Maor, and
A Buchmann, and
W Kunz, and
H C Pitot
May 1999,
Hepatology (Baltimore, Md.),
M Schwarz, and
G Peres, and
D G Beer, and
M Maor, and
A Buchmann, and
W Kunz, and
H C Pitot
September 1989,
FEBS letters,
M Schwarz, and
G Peres, and
D G Beer, and
M Maor, and
A Buchmann, and
W Kunz, and
H C Pitot
January 2019,
Przeglad gastroenterologiczny,
M Schwarz, and
G Peres, and
D G Beer, and
M Maor, and
A Buchmann, and
W Kunz, and
H C Pitot
December 1976,
The Journal of biological chemistry,
M Schwarz, and
G Peres, and
D G Beer, and
M Maor, and
A Buchmann, and
W Kunz, and
H C Pitot
October 1977,
Proceedings of the National Academy of Sciences of the United States of America,
M Schwarz, and
G Peres, and
D G Beer, and
M Maor, and
A Buchmann, and
W Kunz, and
H C Pitot
June 1977,
British journal of cancer,
M Schwarz, and
G Peres, and
D G Beer, and
M Maor, and
A Buchmann, and
W Kunz, and
H C Pitot
January 1993,
Methods in enzymology,
M Schwarz, and
G Peres, and
D G Beer, and
M Maor, and
A Buchmann, and
W Kunz, and
H C Pitot
February 2000,
The American journal of surgical pathology,
M Schwarz, and
G Peres, and
D G Beer, and
M Maor, and
A Buchmann, and
W Kunz, and
H C Pitot
July 1978,
Cancer research,
M Schwarz, and
G Peres, and
D G Beer, and
M Maor, and
A Buchmann, and
W Kunz, and
H C Pitot
April 1987,
Brain research,
