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Comment
. 2010 Nov;1(7):470-471.
doi: 10.18632/oncotarget.183.

A new therapeutic basis for treating Li-Fraumeni Syndrome breast tumors expressing mutated TP53

Robert I Glazer
Comment

A new therapeutic basis for treating Li-Fraumeni Syndrome breast tumors expressing mutated TP53

Robert I Glazer. Oncotarget. 2010 Nov.
No abstract available

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Figures

Figure 1
Figure 1. Survival pathways associated with the Li-Fraumeni mutated TP53 phenotype
Li-Fraumeni Syndrome (LFS) breast epithelial cells heterozygous for TP53 mutation M133T exhibit a marked upregulation of BIRC3 expression. BIRC3 associates with the TNFα receptor 2 (TNFR2)-associated proteins, TRAF1 and TRAF2, to inhibit caspase-3 activation and block apoptosis. Additionally, TRAF1/2 upregulates expression of transcription factor NFκB, which in turn increases BIRC3 expression. LFS stromal cells exhibit upregulation of IL-1β, which induces NFκB, and the secretion of cytokines that further perpetuate NFκB expression and pro-survival signaling.
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