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

被引：108
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
收藏
页码：815 / 822
页数：8
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