['p53 is a 393-residue nuclear phosphoprotein. Mutation of p53 occurs in over half of all human cancers and thus is a crucial step in the process of cell transformation and tumorigenesis. Since tumorigenesis is a multistep process, it generally requires the mutation of certain key oncogenes and/or tumor-suppressor genes. Using p53-deficient mice, we can investigate the p53-dependent mechanisms leading to tumorigenesis.', 'To examine the unique anchorage-independent growth characteristics of dermal fibroblasts isolated from p53-deficient mice.', 'The growth characteristics of highly confluent cultured dermal fibroblasts from wild-type (p53+/+) and p53-deficient (p53-/-) mice were compared by DNA fragmentation assay, colony formation in soft agar, and overexpression of a wild-type p53 transgene in p53-deficient cells.', 'p53-/- fibroblasts have a growth rate dramatically higher than p53+/+ cells and detach from plastic cultureware at high density. The detachment of p53-/- cells is not due to apoptosis. Furthermore, these cells have the capacity to grow in soft agar-a hallmark of cell transformation-and this anchorage-independent growth can be reversed by the introduction of a wild-type p53 transgene.'] Is anchorage-independent growth of p53-knockout dermal fibroblasts reversed by wild-type p53?