TY - JOUR
T1 - Cellular Origin of Androgen Receptor Pathway-Independent Prostate Cancer and Implications for Therapy
AU - Brennen, W. Nathaniel
AU - Isaacs, John T.
N1 - Publisher Copyright:
© 2017 Elsevier Inc.
PY - 2017/10/9
Y1 - 2017/10/9
N2 - 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. 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.
AB - 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. 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.
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U2 - 10.1016/j.ccell.2017.09.011
DO - 10.1016/j.ccell.2017.09.011
M3 - Short survey
C2 - 29017052
AN - SCOPUS:85032921003
SN - 1535-6108
VL - 32
SP - 399
EP - 401
JO - Cancer Cell
JF - Cancer Cell
IS - 4
ER -