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Molecular drivers of metastatic castrate-resistant prostate cancer: New roads to resistance

机译:转移性阉割前列腺癌的分子驱动因素:抵抗的新道路

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摘要

Numerous growth-inducing signaling pathways have been implicated in the development of metastatic castrate-resistant prostate cancer, but their cross-talk with androgen receptor functions remains poorly understood. A recent study published in Science Signaling by Chen et al.(1) has identified a novel androgen-mediated signaling axis driven by loss of SPDEF and gain of TGFBI to facilitate metastasis, which may explain the acquisition of resistance to androgen deprivation therapy. These findings suggest that therapeutic inhibition of androgen signaling may inadvertently promote castrate resistance by inhibiting tumor suppressive functions of the androgen receptor.
机译:许多生长诱导的信号通路已经涉及转移性阉割的前列腺癌的发育,但与雄激素受体功能的串扰仍然明白。 陈等人的科学信号传导中发表的最近研究。(1)已鉴定出一种新的雄激素介导的信号轴,其通过损失SPDEF和TGFBI的增益而推动,以促进转移,这可以解释对雄激素剥夺治疗的抗性的抗性。 这些发现表明,通过抑制雄激素受体的肿瘤抑制功能,可以无意地促进雄激素信号传导的治疗抑制。

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