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Regulation of p53 by protein kinase C during multi-stage carcinogenesis

  • Guest Editorial
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Conclusions

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.

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Authors and Affiliations

  1. Laboratory of Molecular Biology, Institute of General Pathology, University of Firenze, Viale G.B. Morgagni 50, I-50134, Firenze, Italy

    Lucia Magnelli & Vincenzo Chiarugi

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  1. Lucia Magnelli
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  2. Vincenzo Chiarugi
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The Journal Cancer Research and Clinical Oncology occasionally publishes Editorials and Guest editorials on current and controversial problems in experimental and clinical oncology. These papers reflect the personal opinions of the authors. Readers should send any comments directly to the authors.

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Magnelli, L., Chiarugi, V. Regulation of p53 by protein kinase C during multi-stage carcinogenesis. J Cancer Res Clin Oncol 123, 365–369 (1997). https://doi.org/10.1007/BF01240118

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