MYC in Oncogenesis and as a Target for Cancer Therapies

被引:198
作者
Albihn, Ami [1 ]
Johnsen, John Inge [2 ]
Henriksson, Marie Arsenian [1 ]
机构
[1] Karolinska Inst, Dept Microbiol Tumor & Cell Biol MTC, Stockholm, Sweden
[2] Karolinska Inst, Childhood Canc Res Unit, Dept Woman & Childrens Hlth, Stockholm, Sweden
来源
ADVANCES IN CANCER RESEARCH, VOL 107 | 2010年 / 107卷
关键词
CELL LUNG-CANCER; TELOMERASE REVERSE-TRANSCRIPTASE; SMALL-MOLECULE INHIBITORS; ETOPOSIDE-INDUCED APOPTOSIS; HEDGEHOG PATHWAY INHIBITOR; CYCLIN-DEPENDENT KINASES; ESTROGEN-RECEPTOR-ALPHA; EPIDERMAL-GROWTH-FACTOR; PLURIPOTENT STEM-CELLS; EPSTEIN-BARR-VIRUS;
D O I
10.1016/S0065-230X(10)07006-5
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
MYC proteins (c-MYC, MYCN, and MYCL) regulate processes involved in many if not all aspects of cell fate. Therefore, it is not surprising that the MYC genes are deregulated in several human neoplasias as a result from genetic and epigenetic alterations. The near "omnipotency" together with the many levels of regulation makes MYC an attractive target for tumor intervention therapy. Here, we summarize some of the current understanding of MYC function and provide an overview of different cancer forms with MYC deregulation. We also describe available treatments and highlight novel approaches in the pursuit for MYC-targeting therapies. These efforts, at different stages of development, constitute a promising platform for novel, more specific treatments with fewer side effects. If successful a MYC-targeting therapy has the potential for tailored treatment of a large number of different tumors. (C) 2010 Elsevier Inc.
引用
收藏
页码:163 / 224
页数:62
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