Background

The results from the CHAARTED and STAMPEDE trials that docetaxel plus androgen-deprivation therapy (ADT) significantly improves survival over ADT alone among men with metastatic, hormone-sensitive and hormone-naïve prostate cancers, represents a potential practice-changing movement. Clinical data exist to support the role of various predictive markers for taxane response, including low or negative class III beta tubulin (TUBB3), positive transducin-like enhancer of split 3 (TLE3) and low or negative p-glycoprotein (PGP/ABCB1). We examined a database of molecularly-profiled prostate cancer patients for taxane sensitivity markers for insight into the mechanism behind the clinical effect of docetaxel.