NRASG12V oncogene mediates self-renewal in acute myelogenous leukemia
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2013-07-22
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GREB1 amplifies androgen receptor output in prostate cancer and contributes to antiandrogen resistance. GREB1 amplifies androgen receptor output in prostate cancer and contributes to antiandrogen resistance
Genomic amplification of the androgen receptor (AR) is an established mechanism of antiandrogen resistance in prostate cancer. Here we show that the magnitude of AR signaling output, independent of AR
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RUVBL1 promotes enzalutamide resistance of prostate tumors through the PLXNA1-CRAF-MAPK pathway
The aim of this research was to confirm the regulatory effect of RUVBL1 on gene expression in castration resistant prostate cancer. In this research, there were six samples examined including samples
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Glucocorticoid Receptor Confers Resistance to Anti-Androgens by Bypassing Androgen Receptor Blockade.
This SuperSeries is composed of the SubSeries listed below. Overall design: Refer to individual Series
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Drug-induced epigenomic plasticity reprograms circadian rhythm regulation to drive prostate cancer towards androgen-independence [Cell line ChIP-Seq]
In prostate cancer, androgen receptor (AR)-targeting agents are very effective in various stages of the disease. However, therapy resistance inevitably occurs and little is known about how tumor cells
NIAID Data Ecosystem70
Expression data from prostate cancer cell lines C4-2B (enzalutamide sensitive) and C4-2B-MDVR (enzalutamide resistant) cells. Homo sapiens
Prostate cancer C4-2B cells were cultured in enzalutamide in a dose-escalation manner. After sixty passages cells were resistant to enzalutamide, with a specific sets of genes been deregulated. We per
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