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 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.
authors.affiliation: Program in Molecular Therapeutics, Fox Chase Cancer Center, Philadelphia, PA 19111, USA.
authors.forename: Sanjeevani
authors.initials: S
authors.lastname: Arora
authors.affiliation: Program in Molecular Therapeutics, Fox Chase Cancer Center, Philadelphia, PA 19111, USA. erica.golemis@fccc.edu.
authors.forename: Erica A
authors.initials: EA
authors.lastname: Golemis
mesh_terms: D001943:Breast Neoplasms / Q000378:metabolism*; D004721:Endoplasmic Reticulum / Q000378:metabolism*; D005260:Female; D006801:Humans; D020935:MAP Kinase Signaling System; D059748:Proteolysis; D018719:Erb-b2 Receptor Tyrosine Kinases / Q000378:metabolism*; D058570:TOR Serine-Threonine Kinases / Q000378:metabolism*
chemical_list: D018719:Erb-b2 Receptor Tyrosine Kinases; D058570:TOR Serine-Threonine Kinases