癌症研究
多发性骨髓瘤
IRF4公司
染色体易位
MAPK/ERK通路
浆细胞瘤
癌症
生物
机制(生物学)
信号转导
免疫学
转录因子
基因
遗传学
认识论
哲学
作者
Katarina Jovanović,Catherine Roche‐Lestienne,Irene M. Ghobrial,Thierry Façon,Bruno Quesnel,Salomon Manier
出处
期刊:Leukemia
[Springer Nature]
日期:2018-02-21
卷期号:32 (6): 1295-1306
被引量:99
标识
DOI:10.1038/s41375-018-0036-x
摘要
Multiple myeloma (MM) is a plasma cell tumor marked by clonal evolution and preceded by a premalignant stage, which progresses via molecular pathway deregulation, including MYC activation. This activation relates to translocation or gain of the MYC locus and deregulation of upstream pathways such as IRF4, DIS3/LIN28B/let-7, or MAPK. Precision medicine is an approach to predict more accurately which treatment strategies for a particular disease will work in which groups of patients, in contrast to a one-size-fits-all approach. The knowledge of mechanisms responsible for MYC deregulation in MM enables identification of vulnerabilities and therapeutic targets in MYC-driven tumors. MYC can be targeted directly or indirectly, by interacting with several of its functions in cancer. Several such therapeutic strategies are evaluated in clinical trials in MM. In this review, we describe the mechanism of MYC activation in MM, the role of MYC in cancer progression, and the therapeutic options to targeting MYC.
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