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. 2019 Nov 27;2:436. doi: 10.1038/s42003-019-0669-y

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© This is a U.S. government work and not under copyright protection in the U.S.; foreign copyright protection may apply 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 7 — Molecular mechanisms of p53 loss of heterozygosity in breast cancer in response to DNA damage. Proposed model for the role of mutp53 in promoting tumorigenesis. Following DNA damage, p53 expression is induced. Wtp53 would induce cell-cycle arrest and suppression of the mTOR pathway. On the other hand, mutp53 would promote cell-cycle progression with unrepaired DNA, LOH and cell survival via activation of the mTOR pathway through HSF1-HS90 axis, eventually leading to genomic instability, tumor progression, and metastasis.