Department of Oncology, The Sidney Kimmel Comprehensive Cancer Center (SKCCC), The Johns Hopkins School of Medicine, Baltimore, MD 21205, USA.
Department of Oncology, The Sidney Kimmel Comprehensive Cancer Center (SKCCC), The Johns Hopkins School of Medicine, Baltimore, MD 21205, USA; The Brady Urological Institute, The Johns Hopkins School of Medicine, Baltimore, MD 21205, USA.
Cancer Cell. 2017 Oct 9;32(4):399-401. doi: 10.1016/j.ccell.2017.09.011.
In this issue of Cancer Cell, Bluemn et al. report that ∼20% of metastatic castration-resistant prostate cancers express neither AR nor neuroendocrine genes and show AR pathway-independent growth, driven instead by a FGFR/MAPK/ID1 signaling cascade. These results provide a strong rationale for co-targeting AR bypass pathways with initial AR antagonism.
在本期《癌细胞》杂志中，Bluemn 等人报告说，约 20%的转移性去势抵抗性前列腺癌既不表达 AR 也不表达神经内分泌基因，表现出 AR 通路非依赖性生长，而是由 FGFR/MAPK/ID1 信号级联驱动。这些结果为初始 AR 拮抗作用联合靶向 AR 旁路途径提供了强有力的理论依据。
