© 1991 Oxford University Press
research-article |
Control of cell death (apoptosis) by diethylstilbestrol in an estrogen-dependent kidney tumor
Institut für Tumorbiologie-Krebsforschung, University of Vienna Vienna, Austria
1Department of Pharmacology and Toxicology, University of Texas Medical Branch Galveston, TX
2Department of Biochemistry and Molecular Biology, University of Texas Medical School Houston, TX, USA
3Department of Toxicology, Schering AG Berlin, FRG
4Unité de Biochimie Toxicologique et Cancerologique, Université Catholique de Louvain UCL 7369 Bruxelles, Belgium
The role of cell death as a determinant for tumor growth and regression was studied using an estrogen-dependent, trans-plantable kidney tumor designated H301. H301 cells were injected s.c. into diethylstilbestrol(DES)-treated male Syrian hamsters and developed solid tumors of 1–2 g within 2–3 weeks. Upon withdrawal of estrogen the tumors regressed by 80–90% within 4 days. Mitoses, necrotic areas and single-cell death indicated by small, condensed cell residues, were counted in hematoxylin and eosin stained histologkal sections of the tumors. Coincident with tumor regression after DES withdrawal, mitotk activity decreased by 
90%; the rate of single-cell death increased (by 2-fold at its maximum). The incidence of necrotic areas was not affected by DES withdrawal. DES re-treatment resulted in reduction of single-cell death by 80% within 8 h. Mitotic activity increased within 24 h to the level observed before DES withdrawal. Again, the incidence of necrotic areas did not change. As a result, tumors re-grew to their previous size within 2 days after resumption of DES treatment. These results led to the following conclusions: (i) DES treatment inhibits and DES withdrawal enhances single-cell death of H301 tumor cells. (ii) Both this functional property and its morphology characterize single-cell death in the tumors as apoptosis. (iii) Estrogen-dependent cell death determines, in addition to mitosis and necrosis, the growth rate of H301 tumors, (iv) This experimental model may provide a useful tool to study the interaction of potential anti-tumor drugs with apoptosis in neoplasia.
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  A. Yoshida, R. R. Newbold, and D. Dixon Effects of Neonatal Diethylstilbestrol (DES) Exposure on Morphology and Growth Patterns of Endometrial Epithelial Cells in CD-1 Mice Toxicol Pathol, May 1, 1999; 27(3): 325 - 333. [Abstract] [PDF]
|
|
|
|
|
|
R. Schulte-Hermann, W. Bursch, B. Grasl-Kraupp, B. Marian, L. Torok, P. Kahl-Rainer, and A. Ellinger Concepts of Cell Death and Application to Carcinogenesis Toxicol Pathol, January 1, 1997; 25(1): 89 - 93. [Abstract] [PDF]
|
|
|
|
 |
|
 A. Palumbo and J. Yeh Apoptosis as a Basic Mechanism in the Ovarian Cycle: Folicular Atresia and Luteal Regression Reproductive Sciences, May 1, 1995; 2(3): 565 - 573. [Abstract] [PDF]
|
|