Triple negative breast cancer (TNBC) patients have poor prognoses and survival outcomes such that the development of new targeted therapies is in strong demand. Mechanisms associated with high proliferation and aggressive tumor progression, such as PI3K/PTEN aberration, EGFR overexpression, and cell cycle up-regulation, play important roles in TNBC. The molecular chaperone heat shock protein 90 kDa (Hsp90) is required for the conformational maturation and stability of a variety of proteins in multiple pathways, such as EGFR, AKT, Raf, cdk4, etc. Therefore, an Hsp90 inhibitor may demonstrate therapeutic benefit in TNBC by targeting multiple pathways.
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06/29/11