Drug-induced epigenomic plasticity reprograms circadian rhythm regulation to drive prostate cancer towards androgen-independence (ChIP-seq)
|Study ID||Alternative Stable ID||Type|
Understanding how prostate cancer cells adapt to AR-targeted interventions is critical for identifying novel drug targets to improve the clinical management of treatment-resistant disease. Our study revealed an enzalutamide-induced epigenetic plasticity towards pro-survival signaling, and uncovered circadian regulator ARNTL as an acquired vulnerability after AR inhibition, presenting a novel clinical lead for therapeutic development.
Study Datasets 1 dataset.
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ChIP-seq for AR, FOXA1 and H3K27ac in primary prostate tumors before and after 3 months of neoadjuvant enzalutamide treatment. RNA-seq expression data of primary prostate tumors before and after 3 months of neoadjuvant enzalutamide treatment.
|Illumina HiSeq 2500||245|
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