Abstract
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 identifi ed 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 diffi cult class of breast tumors.
| Original language | English |
|---|---|
| Pages (from-to) | fs11 |
| Journal | Science Signaling |
| Volume | 8 |
| Issue number | 378 |
| DOIs | |
| State | Published - May 26 2015 |
UN SDGs
This output contributes to the following UN Sustainable Development Goals (SDGs)
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SDG 3 Good Health and Well-being
Keywords
- Breast Neoplasms/metabolism
- Endoplasmic Reticulum/metabolism
- Female
- Humans
- MAP Kinase Signaling System
- Proteolysis
- Receptor, ErbB-2/metabolism
- TOR Serine-Threonine Kinases/metabolism
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