期刊
SCIENCE SIGNALING
卷 8, 期 378, 页码 -出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/scisignal.aac4746
关键词
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资金
- National Cancer Institute (NCI) [P30 CA006927]
- Temple University Fund for Genomics Research
- NCI [CA181287, CA149147]
- Fox Chase Cancer Center Board
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.
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