The ErbB2/ErbB3 heterodimer functions as an oncogenic unit: ErbB2 requires ErbB3 to drive breast tumor cell proliferation

By Thomas Holbro, R. Beerli, Francisca Maurer, M. Koziczak, C. Barbas, N. Hynes. Proceedings of the National Academy of Sciences of the United States of America, 2003

955 citations recorded by the source corpus.

Subfields: Oncology, Radiology, Nuclear Medicine and Imaging

View Paper: https://www.semanticscholar.org/paper/d90468c306d7097dde5859c13e8d16a500782cbe

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Oncology

1. J. Pollard
2. J. Baselga
3. M. Moasser
4. N. Hynes
5. S. Swain
6. J. Condeelis
7. Gwen Macdonald
8. M. Scaltriti

In Radiology, Nuclear Medicine and Imaging

1. J. Baselga
2. N. Hynes
3. M. Moasser
4. S. Swain
5. Gwen Macdonald
6. M. Sliwkowski
7. J. Pollard
8. M. Lacouture

Citations in the corpus

• Novel anticancer targets: revisiting ERBB2 and discovering ERBB3 (2009, background): “The ERBB2–ERBB3 dimer is crucial for ERBB2-mediated signalling in tumours containing amplifications of ERBB2 (Ref”
• A Paracrine Loop between Tumor Cells and Macrophages Is Required for Tumor Cell Migration in Mammary Tumors (2004, background): “CSF-1 and CSF-1 receptor expression is correlated with invasive mammary tumors in human populations and animal models (40, 41), and CSF-1 is chemotactic for macrophages (38, 42) Heregulin has been shown to enhance motility and migration of cancer cells (43) and, as the ligand for the ErbB2/ErbB3 het”
• The oncogene HER2: its signaling and transforming functions and its role in human cancer pathogenesis (2007, background): “Cell transformation by overexpressed HER2 is also associated with increased HER3 phosphorylation and activation of PI3K/Akt signaling (Alimandi et al., 1995; Wallasch et al., 1995a; Ram and Ethier, 1996; Holbro et al., 2003; Tokunaga et al., 2006).”
• A central role for HER3 in HER2-amplified breast cancer: implications for targeted therapy. (2008, background): “These results confirm and extend the notion that HER2/ HER3 is the major oncogenic unit in breast cancers with HER2 gene amplification (18).”
• ERBB receptors and cancer: the complexity of targeted inhibitors (2005, background): “In particular, are mutations in the ERBB2 kinase domain predictive for clinical response? Considering the proven molecular role of the ERBB2–ERBB3 heterodimer in breast tumour cell lines that overexpress ERBB2 (Ref”
• ErbB receptors and signaling pathways in cancer. (2009, background): “Indeed, the inactivation of ErbB2 in breast cancer cell lines using TKIs or trastuzumab leads to decreased ErbB3 tyrosine phosphorylation and PI3K signaling [31,42].”
• Epidermal Growth Factor Receptor Cell Proliferation Signaling Pathways (2017, background): “However, ERBB3 can still be phosphorylated and induce potent downstream signaling [25].”
• AKT inhibition relieves feedback suppression of receptor tyrosine kinase expression and activity (2011, positive): “In breast cancers, overexpressed HER2 dimerizes with and phosphorylates HER3, which binds to and activates PI3K (Holbro et al., 2003).”
• High-Dimensional Sparse Factor Modeling: Applications in Gene Expression Genomics (2008, background): “…gene is significant and most highly loaded on the ER response factor; this is the HER3 gene, known to play roles in the development of more highly proliferative cellular states in breast cancers (Holbro et al. 2003), as well as biochemically partnering with HER2 in promoting cellular transformation.”
• Ligand-independent HER2/HER3/PI3K complex is disrupted by trastuzumab and is effectively inhibited by the PI3K inhibitor GDC-0941. (2009, methodology): “effects in HER2-positive breast cancer cell lines (Holbro et al., 2003; Ram et al., 2000).”