Abstract
Hormone refractory prostate cancer (HRPC) is heterogeneous and a significant cause of morbidity and mortality. Androgen receptor mutations and amplifications may explain relapse in some patients, but in approximately 70% of cases, alternative mechanisms must be invoked and type I receptor tyrosine kinases may play a role in mediating HRPC. In this study, EGFR and ERBB2 gene amplification and alteration were analyzed in HRPC.
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