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Laboratory of Molecular Virology, National Cancer Institute [B. H., S. D. S.], and Carcinogenesis Intramural Program [A. L. B., J. G. D., M. Z., L. E.], Frederick Cancer Research Center, Frederick, Maryland 21701
A cloned line of BALB/c-derived mouse cells (10E2) was used to compare the phenotypic properties of cells transformed either spontaneously, by UV-irradiated herpes simplex virus (UV-HSV), or by SV40. Cells transformed by SV40 (tumorigenic and nontumorigenic) expressed several in vitro properties usually associated with transformed cells, including: (a) growth in serum-deficient medium; (b) high saturation density and loss of contact inhibition; and (c) anchorage independence in agarose and agar. Tumorigenic cells transformed spontaneously or by UV-HSV were indistinguishable from each other and did not express these properties. The SV40-transformed cells, but not the UV-HSV- or spontaneously transformed cells, also expressed transplantation rejection antigens. No correlation was found between any of the in vitro properties tested and tumor induction by 10E2 cells transformed either spontaneously, by UV-HSV, or by SV40.
No evidence of viral DNA, RNA, or proteins was found in cells transformed by UV-HSV within limitations of the applied techniques. The UV-HSV-transformed cells demonstrated no in vitro properties distinct from spontaneously transformed cells which could be ascribed to retained viral gene sequences. This differed from SV40-transformed cells, where retained viral gene sequences were apparently responsible for expression by the cells of in vitro properties usually associated with a transformed phenotype. The fact that 10E2 cells tumorigenically transformed by UV-HSV differed significantly from cells transformed by SV40 suggested that if a "transforming" segment of the herpes simplex virus genome was retained in the cells, it did not function to alter the in vitro growth properties of the cells, as occurred with SV40-transformed cells.
1 This research was supported by Contract N01-CO-75380 with the National Cancer Institute, NIH, Bethesda, Md. 20205.
2 To whom requests for reprints should be addressed.
Received 1/11/80. Accepted 3/21/80.
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