Epigenetic Control of Gene Expression in the Normal and Malignant Human Prostate: A Rapid Response Which Promotes Therapeutic Resistance

被引:8
作者
Frame, Fiona M. [1 ]
Maitland, Norman J. [1 ]
机构
[1] Univ York, Dept Biol, Canc Res Unit, York YO10 5DD, N Yorkshire, England
关键词
epigenetics; heterogeneity; prostate cancer; differentiation; tumor-initiating cells; CANCER STEM-CELLS; ACUTE MYELOID-LEUKEMIA; DNA-DAMAGE; RNA-SEQ; CHROMATIN-STRUCTURE; ANDROGEN RECEPTOR; INTRATUMORAL HETEROGENEITY; RADIATION-RESISTANCE; CLONAL EVOLUTION; RETINOIC ACID;
D O I
10.3390/ijms20102437
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
A successful prostate cancer must be capable of changing its phenotype in response to a variety of microenvironmental influences, such as adaptation to treatment or successful proliferation at a particular metastatic site. New cell phenotypes emerge by selection from the large, genotypically heterogeneous pool of candidate cells present within any tumor mass, including a distinct stem cell-like population. In such a multicellular model of human prostate cancer, flexible responses are primarily governed not only by de novo mutations but appear to be dominated by a combination of epigenetic controls, whose application results in treatment resistance and tumor relapse. Detailed studies of these individual cell populations have resulted in an epigenetic model for epithelial cell differentiation, which is also instructive in explaining the reported high and inevitable relapse rates of human prostate cancers to a multitude of treatment types.
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