Journal Article

Suppression of apoptosis in C3H mouse liver tumors by activated Ha-<i>ras</i> oncogene

Steffen Frey, Albrecht Buchmann, Wilfried Bursch, Rolf Schulte-Hermann and Michael Schwarz

in Carcinogenesis

Volume 21, issue 2, pages 161-166
Published in print February 2000 | ISSN: 0143-3334
Published online February 2000 | e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/21.2.161
Suppression of apoptosis in C3H mouse liver tumors by activated Ha-ras oncogene

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Liver tumors were induced in male C3H mice by a single injection of N-nitrosodiethylamine and characterized with respect to the presence of base substitutions in the hot-spot position at codon 61 of the Ha-ras proto-oncogene. An increase in Ha-ras mutation prevalence was found with time after induction of tumors, suggesting that the activated ras gene provides a selective growth advantage. However, no significant differences in 5-bromodeoxyuridine labeling indices were evident between ras mutated and ras wild-type tumors, demonstrating that cell division rates in the two tumor populations were very similar. Apoptotic indices were determined by counting eosinophilic apoptotic bodies. The frequency of occurrence of apoptotic bodies was found to be approximately five times lower in tumors with Ha-ras mutations when compared with tumors not showing the mutation. This demonstrates that the activated p21Ras protein has anti-apoptotic activity in transformed mouse hepatocytes in vivo and suggests that the preferential outgrowth of Ha-ras-mutated hepatoma cells is mediated by suppression of apoptosis rather than by stimulation of cell division.

Keywords: BrdUrd, 5-bromodeoxyuridine; DEN, N-nitrosodiethylamine; H&E, hematoxylin and eosin; NFκB, nuclear factor κB; PI3 kinase, phosphatidylinositide 3′-OH kinase.

Journal Article.  4890 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

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