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Infrequent p53 Mutation in Mouse Tumors with Deregulated myc

Pediatrics Branch [M. I. G., K. B., I. T. M.] and Molecular Genetics Section, Laboratory of Genetics [D. S., L. W., J. F. M., K. H.], National Cancer Institute, NIH, Bethesda, Maryland 20892

An invariant genetic lesion in mouse plasmacytomas is deregulated expression of c-myc as a consequence of chromosomal translocation. However, retroviral and transgenic studies suggest that additional genetic lesions may contribute to the genesis of plasmacytomas. The p53 tumor suppressor gene is a likely contributor to this genetic lesion, since there is a high incidence of p53 mutation in Burkitt's lymphomas and B-ALL (L3), both of which contain translocations involving c-myc analogous to those in plasmacytomas. In addition, p53 has been shown to be a transcriptional modulator of c-myc expression. In a survey of 27 mouse plasmacytomas by single-strand conformation polymorphism, we identified a single mutation (3.7% incidence), suggesting that p53 lesions are not frequent contributors to plasmacytomagenesis. A similar study of macrophage-monocyte tumors generated by a c-myc-containing retrovirus also indicates a lack of p53 involvement in deregulated c-myc expression. These results suggest that the specific maturation stage of transformed B-lymphocytes, independent of c-myc deregulation, may be the critical factor which determines the involvement of mutant p53.

¹ To whom requests for reprints should be addressed, at Molecular Genetics Section, Laboratory of Genetics, Building 37, Room 2B-21, National Cancer Institute, NIH, Bethesda, MD 20892.

Received 11/ 8/91. Accepted 12/27/91.