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Abstract:
Stat3 is a transcription factor constitutively active in a large number of breast cancers and other tumors, where it works as a central player in the activation of multiple oncogenic pathways. We developed a method to modulate endogenous Stat3 alternative splicing using modified antisense oligonucleotides, to induce the dominant negative Stat3-beta variant in vitro and in vivo. Switching from the full length Stat3 isoform to the stat3-beta variant leads to increased tumor cell death and complete tumor regression in animal models via a novel modulatory mechanism.
| Limitations: |
 APPROVED FOR PUBLIC RELEASE |
| Description: |
Final rept. 1 Sep 2008-31 Aug 2010 |
| Pages: |
27 |
| Report Date: |
Sep 2010 |
| Contract Number: |
W81XWH-08-1-0528 |
| Report Number: |
A731945 |
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Keywords relating to this report:
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