PDF(Pubmed)
Abstract：
Prostate cancer is the most common non-cutaneous cancer among American men. Multiple mechanisms are involved in tumorigenesis and progression to metastases. While androgen deprivation therapy remains the cornerstone of treatment, progression to castration-resistant disease becomes inevitable. Aberrant pathway activations of PI3K/AKT due to PTEN loss, epithelial-mesenchymal transition pathways, homologous recombination repair, and DNA repair pathway mechanisms of resistance and cross-talk lead to opportunities for therapeutic targeting in metastatic castration-resistant prostate cancer. This review focuses on mechanisms of progression and key trials that evaluate the drugs and combinations that exploit these pathways.
摘要：
前列腺癌是美国男性中最常见的非皮肤癌。肿瘤发生和转移的进展涉及多种机制。虽然雄激素剥夺治疗仍然是治疗的基石，发展为去势抵抗疾病变得不可避免。PTEN丢失导致PI3K/AKT异常通路激活,上皮-间质转化途径，同源重组修复，耐药和串扰的DNA修复途径机制为转移性去势抵抗性前列腺癌的治疗靶向提供了机会。这篇综述的重点是进展机制和评估利用这些途径的药物和组合的关键试验。
