IMR Press / FBL / Volume 15 / Issue 3 / DOI: 10.2741/3669

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article
p53 as the main traffic controller of the cell signaling network
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1 Clinical Experimental Oncology Laboratory, National Cancer Institute “Giovanni Paolo II”, Via Hahnemann, 10 - 70126 Bari, Italy
2 Medical and Experimental Oncology Unit, National Cancer Institute “Giovanni Paolo II”, Via Hahnemann, 10 - 70126 Bari, Italy
3 Section of Medical Oncology, Department of Surgery and Oncology, University of Palermo, Palermo, Italy
4 Infections and Cancer Biology Group, International Agency for Research on Cancer, 150 Cours Albert Thomas, 69372 Lyon Cedex 08, France
Front. Biosci. (Landmark Ed) 2010, 15(3), 1172–1190;
Published: 1 June 2010

Among different pathological conditions that affect human beings, cancer has received a great deal of attention primarily because it leads to significant morbidity and mortality. This is essetnially due to increasing world-wide incidence of this disease and the inability to discover the cause and molecular mechanisms by which normal human cells acquire the characteristics that define cancer cells. Since the discovery of p53 over a quarter of a century ago, it is now recognized that virtually all cell fate pathways of live cells and the decision to die are under the control of p53. Such extensive involvement indicates that p53 protein is acting as a major traffic controller in the cell signaling network. In cancer cells, many cell signaling pathways of normal human cells are rerouted towards immortalization and this is accomplished by the corruption of the main controllers of cell signaling pathways such as p53. This review highlights how p53 signaling activity is altered in cancer cells so that cells acquire the hallmarks of cancer including deregulated infinite self replicative potential.

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