Neuroendocrine Differentiation of Prostate Cancer-An Intriguing Example of Tumor Evolution at Play

被引：83

作者：

Patel, Girijesh Kumar ^{[1
]}

Chugh, Natasha ^{[1
]}

Tripathi, Manisha ^{[1
]}

机构：

[1] Texas Tech Univ, Hlth Sci Ctr, Dept Cell Biol & Biochem, Lubbock, TX 79430 USA

来源：

CANCERS | 2019年 / 11卷 / 10期

关键词：

Androgen deprivation therapy (ADT); cellular plasticity; metastasis; neuroendocrine differentiation (NED); radiation therapy; therapy-induced neuroendocrine prostate cancer (t-NEPC); tumor microenvironment (TME); castration resistant prostate cancer (CRPC); SMALL-CELL CARCINOMA; ANDROGEN RECEPTOR; TRANSCRIPTION FACTOR; MOUSE MODEL; MAST-CELLS; GLUCOCORTICOID-RECEPTOR; N-MYC; MOLECULAR CHARACTERIZATION; THERAPEUTIC MANAGEMENT; ACQUIRED-RESISTANCE;

D O I：

10.3390/cancers11101405

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Our understanding of neuroendocrine prostate cancer (NEPC) has assumed a new perspective in light of the recent advances in research. Although classical NEPC is rarely seen in the clinic, focal neuroendocrine trans-differentiation of prostate adenocarcinoma occurs in about 30% of advanced prostate cancer (PCa) cases, and represents a therapeutic challenge. Even though our knowledge of the mechanisms that mediate neuroendocrine differentiation (NED) is still evolving, the role of androgen deprivation therapy (ADT) as a key driver of this phenomenon is increasingly becoming evident. In this review, we discuss the molecular, cellular, and therapeutic mediators of NED, and emphasize the role of the tumor microenvironment (TME) in orchestrating the phenotype. Understanding the role of the TME in mediating NED could provide us with valuable insights into the plasticity associated with the phenotype, and reveal potential therapeutic targets against this aggressive form of PCa.

引用

页数：27

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