The N-myc Oncogene: Maximizing its Targets, Regulation, and Therapeutic Potential

被引：114

作者：

Beltran, Himisha ^{[1
]}

机构：

[1] Weill Cornell Med Coll, New York, NY 10005 USA

来源：

MOLECULAR CANCER RESEARCH | 2014年 / 12卷 / 06期

关键词：

IN-SITU HYBRIDIZATION; DEACETYLASE INHIBITOR BL1521; SMALL-MOLECULE INHIBITORS; SMALL-CELL-CARCINOMA; GENE AMPLIFICATION; C-MYC; DIFFERENTIAL EXPRESSION; ORNITHINE-DECARBOXYLASE; MALIGNANT PROGRESSION; EMBRYONIC LETHALITY;

D O I：

10.1158/1541-7786.MCR-13-0536

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

N-myc (MYCN), a member of the Myc family of basic-helix-loop-helix-zipper (bHLHZ) transcription factors, is a central regulator of many vital cellular processes. As such, N-myc is well recognized for its classic oncogenic activity and association with human neuroblastoma. Amplification and overexpression of N-myc has been described in other tumor types, particularly those of neural origin and neuroendocrine tumors. This review outlines N-myc's contribution to normal development and oncogenic progression. In addition, it highlights relevant transcriptional targets and mechanisms of regulation. Finally, the clinical implications of N-Myc as a biomarker and potential as a target using novel therapeutic approaches are discussed. (C) 2014 AACR.

引用

页码：815 / 822

页数：8

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