Reversion of tumorigenicity and decreased agarose clonability after EBV conversion of an igh/myc translocation‐carrying be line

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Abstract
The Epstein‐Barr virus (EBV)‐negative Burkitt lymphoma (BL) line BL‐41, and 5 independently established EBV‐converted sublines, derived by infection with a transforming (B95‐8) or a nontransforming (P3HRI) strain of EBV, were compared for clonability in semi‐solid agarose and for tumorigenicity in immuno‐suppressed mice. One P3HRI viral convertant and 3 out of 4 B95‐8 virus‐converted sublines had a high (>40%) agarose clonability, like the BL 41 parent, and were slightly more tumorigenic than BL‐41. In contrast, the fourth B95‐8 converted subline, BL‐41/95, was virtually non‐tumorigenic and its agarose clonability was much lower (3–23%). It showed a more drastic shift towards an LCL‐like phenotype than the other convertants as reflected by high HLA class‐I and EBV‐encoded latent membrane protein (LMP) expression. BL 41/95 still contains the 8;14 IgH/myc translocation, carried by the parental line, and maintains the same relatively high steady‐state level of c‐myc mRNA and protein as the highly tumorigenic convertants. We conclude that the tumorigenicity of BL41/95 has been suppressed by a gene that acts at a level beyond the expression of the activated oncogene, in the same way as the revertants isolated from ras and SV‐40‐transformed cultures (Klein, 1987b; Bassin and Noda, 1987).