IMR Press / FBL / Volume 12 / Issue 11 / DOI: 10.2741/2378

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 in breast cancer: mutation and countermeasures
Show Less
1 Department of Pharmacology and Cancer Institute, Southern Illinois University School of Medicine, PO Box 19629, Springfield, IL 62702, USA
Academic Editor:Kounosuke Watabe
Front. Biosci. (Landmark Ed) 2007, 12(11), 4168–4178;
Published: 1 May 2007
(This article belongs to the Special Issue Pathogenesis of tumor progression in breast and prostate cancer)

p53 is the primary arbiter of the mammalian cell's response to stress, the governor of life and death. It is the nexus upon which signals converge from an array of sensors that detect damage to DNA or to the mitotic spindle or the cytoskeleton, hypoxia, cell detachment, growth factor deprivation, oncogene expression and other forms of stress. Depending on the type, intensity and duration of the signals, p53 in turn transactivates batteries of genes specifying cell cycle arrest, DNA repair, apoptosis, or other anti-neoplastic functions. At the same time, p53 represses anti-apoptotic and survival functions. The type, intensity and duration of signaling dictate the sequellae. While this response is combinatorial, the frequent perturbation of p53 function in a wide spectrum of cancers attests to its central role in the suppression of neoplasia. As our understanding of regulation by and of p53 has deepened, many possibilities have been suggested for re-establishing p53 or its effectors in tumor cells. This review will briefly summarize the role of p53 mutations in the etiology and treatment of breast cancer and then consider the wide array of strategies being developed to re-establish p53 function in tumor cells.

Breast Cancer
Back to top