A new strategy to ERADicate HER2-positive breast tumors?

Sanjeevani Arora; Erica A. Golemis

doi:10.1126/scisignal.aac4746

A new strategy to ERADicate HER2-positive breast tumors?

Sanjeevani Arora, Erica A. Golemis

Research output: Contribution to journal › Article › peer-review

3 Scopus citations

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	https://doi.org/10.1126/scisignal.aac4746 https://doi.org/10.1126/scisignal.aac4746s
State	Published - May 26 2015

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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Cite this

@article{6abb07f680604425b80b74e9d4a999ab,

title = "A new strategy to ERADicate HER2-positive breast tumors?",

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.",

keywords = "Breast Neoplasms/metabolism, Endoplasmic Reticulum/metabolism, Female, Humans, MAP Kinase Signaling System, Proteolysis, Receptor, ErbB-2/metabolism, TOR Serine-Threonine Kinases/metabolism",

author = "Sanjeevani Arora and Golemis, {Erica A.}",

note = "Publisher Copyright: Copyright {\textcopyright} 2015 by the American Association for the Advancement of Science.",

year = "2015",

month = may,

day = "26",

doi = "10.1126/scisignal.aac4746",

language = "English",

volume = "8",

pages = "fs11",

journal = "Science Signaling",

issn = "1945-0877",