The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
Epidermal Growth Factor Receptor Mutations in Non–Small-Cell Lung Cancer: Implications for Treatment and Tumor Biology
Abstract
The epidermal growth factor receptor (EGFR) has emerged as an attractive therapeutic target for patients with non–small-cell lung cancer (NSCLC). However, despite its almost universal presence in NSCLC tumors, therapeutic inhibition of EGFR has resulted in significant tumor regressions in only 10% to 20% of patients. Several investigations over the last 12 months have uncovered somatic mutations in EGFR that underlie the sensitivity to EGFR inhibitors. NSCLC tumors and cell lines with EGFR mutations are exquisitely sensitive to the EGFR tyrosine kinase inhibitors (TKIs), erlotinib and gefitinib, and are biologically distinct from other forms of NSCLC. Somatic mutations in EGFR are found more frequently in patients with adenocarcinomas, nonsmokers, patients of Asian ethnicity, and in females. EGFR mutation detection is now becoming clinically available and is being incorporated into clinical treatment decisions and into the design of future clinical trials. Mutations in K-ras, a mediator of EGFR signaling, are mutually exclusive with EGFR mutations, and are associated with resistance to EGFR TKIs. In addition, secondary mutations, conferring resistance to EGFR TKIs, in patients with primary EGFR mutations once sensitive to EGFR TKIs, are beginning to be identified. The frequency of EGFR mutations, their impact on NSCLC biology, clinical treatment, and clinical trial design, as well as methods and limitations for mutation detection, will be reviewed.
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EGFR Mutations in Lung Cancer: Correlation with Clinical Response to Gefitinib Therapy
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Clinical Resistance to STI-571 Cancer Therapy Caused by BCR-ABL Gene Mutation or Amplification
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Cited by
Epidermal growth factor receptor mutations in lung cancer
Sharma, S. V., Bell, D. W., Settleman, J., & Haber, D. A. (2007) · Nature Reviews Cancer · doi:10.1038/nrc2088 · Cited by 3,170
BIBW2992, an irreversible EGFR/HER2 inhibitor highly effective in preclinical lung cancer models
Li, D., Ambrogio, L., Shimamura, T., Kubo, S., Takahashi, M., Chirieac, L. R., Padera, R. F., Shapiro, G. I., Baum, A., Himmelsbach, F., et al. (2008) · Oncogene · doi:10.1038/onc.2008.109 · Cited by 1,447
Khambata-Ford, S., Garrett, C. R., Meropol, N. J., Basik, M., Harbison, C. T., Wu, S., Wong, T. W., Huang, X., Takimoto, C. H., Godwin, A. K., et al. (2007) · Journal of Clinical Oncology · doi:10.1200/jco.2006.10.5437 · Cited by 1,125
Mechanisms of receptor tyrosine kinase activation in cancer
Du, Z., & Lovly, C. M. (2018) · Molecular Cancer · doi:10.1186/s12943-018-0782-4 · Cited by 1,066
Treatment of Medulloblastoma with Hedgehog Pathway Inhibitor GDC-0449
Rudin, C. M., Hann, C. L., Laterra, J., Yauch, R. L., Callahan, C. A., Fu, L., Holcomb, T., Stinson, J., Gould, S. E., Coleman, B., et al. (2009) · New England Journal of Medicine · doi:10.1056/nejmoa0902903 · Cited by 1,019
Metadata
- Authors
- Jänne, P. A., Engelman, J. A., & Johnson, B. E.
- Venue
- Journal of Clinical Oncology
- Published
- 2005-05-10
- Volume
- 23
- Issue
- 14
- Pages
- 3227-3234
- ISSN
- 0732-183X (ISSN-L)
- 1527-7755
- OpenAlex
- W2059780149
- Cited by
- 405
- References
- 7
- FWCI
- 33.05
- Type
- journal article
- Language
- en
- Open access
- closed
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- Jänne, P. A., Engelman, J. A., & Johnson, B. E. (2005). Epidermal Growth Factor Receptor Mutations in Non–Small-Cell Lung Cancer: Implications for Treatment and Tumor Biology. Journal of Clinical Oncology. https://doi.org/10.1200/jco.2005.09.985
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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.
