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Plos Biology : Treatment of Terminal Peritoneal Carcinomatosis by a Transducible P53-activating Peptide, Volume 2

By Hastie, Nicholas

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Book Id: WPLBN0003923097
Format Type: PDF eBook :
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Reproduction Date: 2015

Title: Plos Biology : Treatment of Terminal Peritoneal Carcinomatosis by a Transducible P53-activating Peptide, Volume 2  
Author: Hastie, Nicholas
Volume: Volume 2
Language: English
Subject: Journals, Science, Biology
Collections: Periodicals: Journal and Magazine Collection (Contemporary), PLoS Biology
Historic
Publication Date:
Publisher: Plos

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Hastie, N. (n.d.). Plos Biology : Treatment of Terminal Peritoneal Carcinomatosis by a Transducible P53-activating Peptide, Volume 2. Retrieved from http://netlibrary.net/


Description
Description : Advanced-stage peritoneal carcinomatosis is resistant to current chemotherapy treatment and, in the case of metastatic ovarian cancer, results in a devastating 15%–20% survival rate. Therapeutics that restore genes inactivated during oncogenesis are predicted to be more potent and specific than current therapies. Experiments with viral vectors have demonstrated the theoretical utility of expressing the p53 tumor suppressor gene in cancer cells. However, clinically useful alternative approaches for introducing p53 activity into cancer cells are clearly needed. It has been hypothesized that direct reactivation of endogenous p53 protein in cancer cells will be therapeutically beneficial, but few tests of this hypothesis have been carried out in vivo. We report that a transducible D-isomer RI-TATp53C9 peptide activates the p53 protein in cancer cells, but not normal cells. RI-TATp53C9 peptide treatment of preclinical terminal peritoneal carcinomatosis and peritoneal lymphoma models results in significant increases in lifespan (greater than 6- fold) and the generation of disease-free animals. These proof-of-concept observations show that specific activation of endogenous p53 activity by a macromolecular agent is therapeutically effective in preclinical models of terminal human malignancy. Our results suggest that TAT-mediated transduction may be a useful strategy for the therapeutic delivery of large tumor suppressor molecules to malignant cells in vivo.

 

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