A new strategy to ERADicate HER2-positive breast tumors?

被引：3

作者：

Arora, Sanjeevani ^{[1
]}

Golemis, Erica A. ^{[1
]}

机构：

[1] Fox Chase Canc Ctr, Program Mol Therapeut, Philadelphia, PA 19111 USA

来源：

SCIENCE SIGNALING | 2015年 / 8卷 / 378期

关键词：

PATHWAY; INHIBITOR; STRESS;

D O I：

10.1126/scisignal.aac4746

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

HER2-positive breast cancers that have become resistant to HER2-targeting agents, such as trastuzumab (also known as Herceptin), have limited treatment options. In this issue of Science Signaling, Singh et al. have identified a characteristic increase in the endoplasmic reticulum (ER)-associated degradation (ERAD) system in HER2-positive tumors as a mechanism of relieving proteotoxic stress. Synthetic lethality arising from targeted disruption of ERAD signaling in conjunction with other HER2-dependent signaling may improve therapeutic management of this difficult class of breast tumors.

引用

页数：2

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