A new trick of an old molecule: androgen receptor splice variants taking the stage?!

A new trick of an old molecule: androgen receptor splice variants taking the stage?!
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DOI:
10.7150/ijbs.7.815
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发表时间:
2011
影响因子:
9.2
通讯作者:
Qiu Y
Qiu Y
中科院分区:
生物学2区
文献类型:
--
作者:
Guo Z;Qiu Y

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前列腺癌是美国男性癌症相关死亡的第二大原因。虽然大多数前列腺癌最初是雄激素依赖的,对雄激素消融治疗有反应,但大多数最终会复发并进展为无法治愈的去势抵抗(或激素耐药)前列腺癌。潜在的机制是深入研究的重点,以开发更有效的治疗方法。来自临床和基础研究的越来越多的证据表明,雄激素受体(AR)的活性仍然是耐去势前列腺癌所必需的。雄激素耗竭条件下AR被重新激活的多种机制可能参与了去势抵抗的发展。最近发现的AR剪接变异体可能会在AR生物学中增加另一层复杂性。现就AR剪接变异体在前列腺癌中的研究进展作一综述。
Prostate cancer is the second leading cause of cancer-related death in American men. Although most prostate cancers are initially androgen-dependent and respond to androgen ablation therapy, majority of them eventually relapse and progress into incurable castration-resistant (or hormone refractory) prostate cancer. The underlying mechanisms are the focus of intensive investigation for development of more effective treatment. Mounting evidence from both clinical and basic research has demonstrated that the activity of the androgen receptor (AR) is still required for castration-resistant prostate cancer. Multiple mechanisms by which AR is re-activated under androgen-depleted conditions may be involved in the development of castration resistance. The recent identification of AR splicing variants may add another layer of complexity in AR biology. The present review summarizes recent progress in study of AR splicing variants in prostate cancer.
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发表时间: 2004-01-01
期刊: NATURE MEDICINE
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