Abstract
Nyquist et al. demonstrate that TP53 and RB1 loss in prostate carcinoma (PC) attenuates AR signaling and enhances cell proliferation but does not uniformly induce neuroendocrine phenotypes. PCs with TP53/RB1 loss resist a wide range of cancer therapeutics but respond to PARP and ATR inhibition, likely reflecting enhanced replication stress.
Original language | English (US) |
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Article number | 107669 |
Journal | Cell Reports |
Volume | 31 |
Issue number | 8 |
DOIs | |
State | Published - May 26 2020 |
Keywords
- ATR
- DNA damage
- PARP
- RB1
- TP53
- androgen receptor
- antiandrogen
- neuroendocrine
- plasticity
- prostate cancer
ASJC Scopus subject areas
- General Biochemistry, Genetics and Molecular Biology