This Article Order Full text via Infotrieve Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Lee, G. H. Search for Related Content PubMed PubMed Citation Articles by Lee, G. H.

American Journal of Pathology, Vol 151, 957-961, Copyright © 1997 by American Society for Investigative Pathology

REGULAR ARTICLES

Correlation between Bcl-2 expression and histopathology in diethylnitrosamine-induced mouse hepatocellular tumors

GH Lee
Department of Pathology, Asahikawa Medical College, Hokkaido, Japan.

It is generally accepted that suppression of apoptosis in chemically initiated hepatocytes results in promotion of rodent hepatocarcinogenesis. Using immuno-histochemical methods, I studied the expression of Bcl-2, an anti-apoptotic protein, in hepatocellular tumors of B6C3F1 mice. Although normal mouse hepatocytes did not express detectable amounts of Bcl-2, most diethylnitrosamine-induced tumors were positive for this protein. Virtually all of the Bcl-2- positive tumors were composed of small basophilic hepatocytes, whereas the rare cases of Bcl-2-negative tumors demonstrated an eosinophilic appearance. To confirm this difference, tumors initiated with diethylnitrosamine and promoted by phenobarbital were also studied, as this initiation-promotion protocol has been shown to selectively produce eosinophilic lesions. All such tumors were immunohistochemically negative for Bcl-2. The relatively infrequent basophilic tumors found with phenobarbital treatment, however, did express Bcl-2. Thus, the concordance with basophilia was observed regardless of the nature of the promotion agent. These results indicate that the two types of tumors are qualitatively distinct and may develop through independent mechanisms.

This article has been cited by other articles:

				M. Iida, C. H. Anna, J. Hartis, M. Bruno, B. Wetmore, J. R. Dubin, S. Sieber, L. Bennett, M. L. Cunningham, R. S. Paules, et al. Changes in global gene and protein expression during early mouse liver carcinogenesis induced by non-genotoxic model carcinogens oxazepam and Wyeth-14,643 Carcinogenesis, April 1, 2003; 24(4): 757 - 770. [Abstract] [Full Text] [PDF]

				J. M. Bugni, T. M. Poole, and N. R. Drinkwater The little mutation suppresses DEN-induced hepatocarcinogenesis in mice and abrogates genetic and hormonal modulation of susceptibility Carcinogenesis, November 1, 2001; 22(11): 1853 - 1862. [Abstract] [Full Text] [PDF]

				M. Iida, H. Iwata, H. Inoue, M. Enomoto, N. Horie, and K. Takeishi Correlation between Bcl-2 Overexpression and H-ras Mutation in Naturally Occurring Hepatocellular Proliferative Lesions of the B6C3F1 Mouse Toxicol. Sci., August 1, 2000; 56(2): 297 - 302. [Abstract] [Full Text] [PDF]

				G.-H. Lee Review Article: Paradoxical Effects of Phenobarbital on Mouse Hepatocarcinogenesis Toxicol Pathol, March 1, 2000; 28(2): 215 - 225. [Abstract] [PDF]

				J. G. Christensen, E. H. Romach, L. N. Healy, A. J. Gonzales, S. P. Anderson, D. E. Malarkey, J. C. Corton, T. R. Fox, R. C. Cattley, and T. L. Goldsworthy Altered bcl-2 family expression during non-genotoxic hepatocarcinogenesis in mice Carcinogenesis, August 1, 1999; 20(8): 1583 - 1590. [Abstract] [Full Text] [PDF]