Abstract
The hypothesis that we are currently trying to demonstrate is that of “initial cells” start the process of carcinogenesis by inducing G1-cyclin-dependent RB phosphorylation, E2F release and an increase of glycolysis, with the consequent sustained diacylglycerol production: PKC is down-regulated and p53 is maintained in its latent, inactive form; genomic damage progressively accumulates and the chromosomal aberrations may activate other oncogenes or deactivate tumor suppressors, leading to progression towards malignancy. This model agrees with the abnormally high level of diacylglycerol found in a variety of malignant tumors (Mills et al. 1993, Hendickse et al. 1995; Casamassima et al. 1996) (see Fig. 1B). To take an extreme view, not only are the presence, the loss, or the mutations sufficient screening data for the status of p53 in malignancy, but also the presence or the absence of phosphate groups at the carboxyl ends, as revealed by Pab421 antibody.