The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.
Critical Update and Emerging Trends in Epidermal Growth Factor Receptor Targeting in Cancer
Open accessAbstract
The epidermal growth factor receptor (EGFR) is a receptor tyrosine kinase of the ErbB receptor family that is abnormally activated in many epithelial tumors. The aberrant activation of the EGFR leads to enhanced proliferation and other tumor-promoting activities, which provide a strong rationale to target this receptor family. There are two classes of anti-EGFR agents: monoclonal antibodies (MAbs) directed at the extracellular domain of the receptor and small molecule, adenosine triphosphate–competitive inhibitors of the receptor's tyrosine kinase. Anti-EGFR MAbs have shown antitumor activity in advanced colorectal carcinoma, squamous cell carcinomas of the head and neck, non–small-cell lung cancer (NSCLC) and renal cell carcinomas. The tyrosine kinase inhibitors (TKIs) have a partially different activity profile. They are active against NSCLC, and a specific EGFR inhibitor has shown improvement in survival. Recently, mutations and amplifications of the EGFR gene have been identified in NSCLC and predict for enhanced sensitivity to anti-EGFR TKIs. In addition to specific anti-EGFR TKIs, there are broader acting inhibitors such as dual EGFR HER-2 inhibitors and combined anti-pan-ErbB and antivascular endothelial growth factor receptor inhibitors. Current research efforts are directed at selecting the optimal dose and schedule and identifying predictive factors of response and resistance beyond EGFR gene mutations and/or amplifications. Finally, there is a need for improved strategies to integrate anti-EGFR agents with conventional therapies and to explore combinations with other molecular targeted approaches including other antireceptor therapies, receptor-downstream signaling transduction inhibitors, and targeted approaches interfering with other essential drivers of cancer, such as angiogenesis.
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Self-citationThe Epidermal Growth Factor Receptor Pathway: A Model for Targeted Therapy
Scaltriti, M., & Baselga, J. (2006) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-05-1554 · Cited by 913
Self-citationAl-Nedawi, K., Meehan, B., Kerbel, R. S., Allison, A. C., & Rak, J. (2009) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0804543106 · Cited by 668
Mechanisms of acquired resistance to cetuximab: role of HER (ErbB) family members
Wheeler, D. L., Huang, S., Kruser, T. J., Nechrebecki, M. M., Armstrong, E. A., Benavente, S., Gondi, V, Hsu, K.-T., & Harari, P. M. (2008) · Oncogene · doi:10.1038/onc.2008.19 · Cited by 550
Metadata
- Authors
- Baselga, J., & Arteaga, C. L.
- Venue
- Journal of Clinical Oncology
- Published
- 2005-04-10
- Volume
- 23
- Issue
- 11
- Pages
- 2445-2459
- ISSN
- 0732-183X (ISSN-L)
- 1527-7755
- OpenAlex
- W2139819066
- Cited by
- 725
- References
- 11
- FWCI
- 40.84
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Baselga, J., & Arteaga, C. L. (2005). Critical Update and Emerging Trends in Epidermal Growth Factor Receptor Targeting in Cancer. Journal of Clinical Oncology. https://doi.org/10.1200/jco.2005.11.890
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
