首页|Prostate Cancer Epigenetic Plasticity and Enhancer Heterogeneity: Molecular Causes, Consequences and Clinical Implications
Prostate Cancer Epigenetic Plasticity and Enhancer Heterogeneity: Molecular Causes, Consequences and Clinical Implications
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Prostate cancer (PCa) proliferation is dictated by androgen receptor (AR) signaling, which regulates gene expression through cis-regulatory regions including proximal and distal enhancers. The repertoire of AR interactions at enhancers is dependent on tissue and cellular contexts and thus shape a spectrum of phe-notypes through such epigenetic heterogeneity. Moreover, PCa is a multifocal disease and displays a high degree of intra- and inter-tumor heterogeneity, adding to the phenotypic complexity. It is increasingly becoming clear that PCa may be considered an epigenetic disease caused by various molecular causes with profound consequences and clinical implications which are underpinned by enhancer interaction heterogeneity.
Prostate cancerEnhancersAndrogen receptorEpigeneticsHeterogeneityCistrome plasticityPersonalized medicine
Jeroen Kneppers、Andries M. Bergman、Wilbert Zwart
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Division of Oncogenomics, Oncode Institute, Netherlands Cancer Institute, Amsterdam, The Netherlands
NSTL
