Abstract
Up to one third of all breast cancers are classified as the aggressive HER2-positive subtype, which is associated with a higher risk of recurrence compared to HER2-negative breast cancers. The HER2 hyperactivity associated with this subtype drives tumor growth by up-regulation of mechanistic target of rapamycin (mTOR) pathway activity and a metabolic shift to glycolysis. Although inhibitors targeting the HER2 receptor have been successful in treating HER2-positive breast cancer, anti-HER2 therapy is associated with a high risk of recurrence and drug resistance due to stimulation of the PI3K-Akt-mTOR signaling pathway and glycolysis. Combination therapies against HER2 with inhibition of mTOR improve clinical outcomes compared to HER2 inhibition alone. Here, we review the role of the HER2 receptor, mTOR pathway, and glycolysis in HER2-positive breast cancer, along with signaling mechanisms and the efficacy of treatment strategies of HER2-positive breast cancer.
| Original language | English |
|---|---|
| Article number | 2922 |
| Journal | Cancers |
| Volume | 13 |
| Issue number | 12 |
| DOIs | |
| Publication status | Published - Jun 2 2021 |
Bibliographical note
Funding Information:Funding: The authors acknowledge funding support from the Dalhousie Medical Research Foundation and the Breast Cancer Society of Canada.
Publisher Copyright:
© 2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https:// creativecommons.org/licenses/by/ 4.0/).
ASJC Scopus Subject Areas
- Oncology
- Cancer Research
PubMed: MeSH publication types
- Journal Article
- Review
