作者: Yao Huang , Yongchang Chang
DOI: 10.5772/27021
关键词:
摘要: The molecular mechanisms of prostate cancer are still poorly understood, despite the threat that poses to health men worldwide. As tumors initially dependent on androgens for growth and survival, androgen deprivation therapy is firstline treatment patients. However, a hormonal-refractory (androgen independent) state often develops afterwards, principal options palliative because tumor progression, which characterized by uncontrolled metastasis associated with independence. To date, no effective can abrogate progression advanced, invasive forms. Recent evidence suggests acquisition androgen-independence may be due upregulation factor receptor signaling pathways, principally epidermal (EGFR)/ErbB/human (HER) family (Craft et al., 1999), making it an attractive target therapeutic intervention. EGFR/ErbB/HER in has been extensively studied decades, there have number excellent reviews roles ErbB receptors initiation wide variety cancers, including (Laskin & Sandler, 2004; Ratan 2003; Yarden Sliwkowski, 2001). Thus, this review chapter will focus more narrowly EGFR phosphorylation, signaling, trafficking, their specific development (tumor metastasis) given growing literature area. Better understanding precise divergent pathways phenotypic consequences (and normal prostate) enable selective therapies urologic disease.