The DOI matches its Crossref record; 83 of the 83 references it cites were found in a registry or an index.
Status of Epidermal Growth Factor Receptor Antagonists in the Biology and Treatment of Cancer
Abstract
The epidermal growth factor receptor (EGFR) is a tyrosine kinase receptor of the ErbB family that is abnormally activated in many epithelial tumors. Receptor activation leads to recruitment and phosphorylation of several downstream intracellular substrates, leading to mitogenic signaling and other tumor-promoting cellular activities. In human tumors, receptor overexpression correlates with a more aggressive clinical course. Taken together, these observations indicate that the EGFR is a promising target for cancer therapy. Monoclonal antibodies directed at the ligand-binding extracellular domain and low–molecular weight inhibitors of the receptor’s tyrosine kinase are currently in advanced stages of clinical development. These agents prevent ligand-induced receptor activation and downstream signaling, which results in cell cycle arrest, promotion of apoptosis, and inhibition of angiogenesis. They also enhance the antitumor effects of chemotherapy and radiation therapy. In patients, anti-EGFR agents can be given safely at doses that fully inhibit receptor signaling, and single-agent activity has been observed against a variety of tumor types, including colon carcinoma, non–small-cell lung cancer, head and neck cancer, ovarian carcinoma, and renal cell carcinoma. Although antitumor activity is significant, responses have been seen in only a minority of the patients treated. In some clinical trials, anti-EGFR agents enhanced the effects of conventional chemotherapy and radiation therapy. Ongoing research efforts are directed at the selection of patients with EGFR-dependent tumors, identification of the differences among the various classes of agents, and new clinical development strategies.
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Cites
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Cited by
Integrative Analysis of Complex Cancer Genomics and Clinical Profiles Using the cBioPortal
Gao, J., Aksoy, B. A., Dogrusoz, U., Dresdner, G., Gross, B., Sumer, S. O., Sun, Y., Jacobsen, A., Sinha, R., Larsson, E., et al. (2013) · Science Signaling · doi:10.1126/scisignal.2004088 · Cited by 15,160
EGFR Mutation and Resistance of Non–Small-Cell Lung Cancer to Gefitinib
Kobayashi, S., Boggon, T. J., Dayaram, T., Jänne, P. A., Kocher, O., Meyerson, M., Johnson, B. E., Eck, M. J., Tenen, D. G., & Halmos, B. (2005) · New England Journal of Medicine · doi:10.1056/nejmoa044238 · Cited by 3,964
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Su, K.-Y., Chen, H.-Y., Li, K.-C., Kuo, M.-L., Yang, J. C.-H., Chan, W.-K., Ho, B.-C., Chang, G.-C., Shih, J.-Y., Yu, S.-L., et al. (2012) · Journal of Clinical Oncology · doi:10.1200/jco.2011.38.3224 · Cited by 499
Metadata
- Authors
- Mendelsohn, J., & Baselga, J.
- Venue
- Journal of Clinical Oncology
- Published
- 2003-07-15
- Volume
- 21
- Issue
- 14
- Pages
- 2787-2799
- ISSN
- 0732-183X (ISSN-L)
- 1527-7755
- OpenAlex
- W2039633811
- Cited by
- 1,255
- References
- 83
- FWCI
- 45.26
- Type
- journal article
- Language
- en
- Open access
- closed
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