Therapy-Induced Developmental Reprogramming of Prostate Cancer Cells and Acquired Resistance
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Therapy-Induced Developmental Reprogramming of Prostate Cancer Cells and Acquired Resistance
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创建时间：
2016-03-11
相关数据集
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
NIAID Data Ecosystem70
Depletion of Nrf2 in pancreatic cancer cells shifts arginine metabolism into the phosphocreatine energy system. Depletion of Nrf2 in pancreatic cancer cells shifts arginine metabolism into the phosphocreatine energy system
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SCL , LMO1 and Notch1 Reprogram Thymocytes into Self-Renewing Cells
The molecular determinants that render specific populations of normal cells susceptible to oncogenic reprogramming into self-renewing cancer stem cells are poorly understood. Here, we exploit T-cell a
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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
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Deep Quantitative Proteomics Reveals Extensive Metabolic Reprogramming and Cancer-Like Changes of Ectopic Endometriotic Stromal Cells
Endometriosis is a prevalent health condition in women of reproductive age characterized by ectopic growth of endometrial-like tissue in the extrauterine environment. Thorough understanding of the mol
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