SPECIFIC AIMSThe aim of this study was to elucidate the contribution, if any, of the tumor suppressor function of p53 to the process of hepatocellular carcinoma (HCC) formation in mice. Its role within networks controlling either cell proliferation or cell death during deterministic liver tumorigenesis in mice overexpressing in the liver transgenes encoding murine c-myc, or c-myc plus the secretable human epidermal growth factor (EGF) analog IgEGF was analyzed.PRINCIPAL FINDINGS1. Lack of p53 caused an increase of relative liver weight in c-myc and c-myc/IgEGF transgenics as well as reduced life spans in c-myc/IgEGF transgenicsp53-deficient c-myc and c-myc/IgEGF transgenics exhibited ∼twofold increased relative liver weight compared with age-matched c-myc/p53+/+ and c-myc/IgEGF/p53+/+ mice.In contrast, the relative weight of IgEGF/p53KO mouse livers remained unchanged compared with their p53 positive counterparts, indicating that a lack of the p53 tumor suppressor function caused increased hepatocyte grow...