The DOI matches its Crossref record; 180 of the 182 references it cites were found in a registry or an index.
Epidermal growth factor receptor mutations in lung cancer
Abstract
The development and clinical application of inhibitors that target the epidermal growth factor receptor (EGFR) provide important insights for new lung cancer therapies, as well as for the broader field of targeted cancer therapies. We review the results of genetic, biochemical and clinical studies focused on somatic mutations of EGFR that are associated with the phenomenon of oncogene addiction, describing 'oncogenic shock' as a mechanistic explanation for the apoptosis that follows the acute treatment of susceptible cells with kinase inhibitors. Understanding the genetic heterogeneity of epithelial tumours and devising strategies to circumvent their rapid acquisition of resistance to targeted kinase inhibitors are essential to the successful use of targeted therapies in common epithelial cancers.
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“Overexpression or increased activity of wild-type EGFR protein can lead to cell proliferation, migration, survival, and anti-apoptosis through signaling cascades, which are strongly associated with the occurrence and development of many cancers, such as NSCLC, breast cancer, glioma, head and neck cancer, cervical cancer, and bladder cancer.105–108”
From Recent advances in targeting the “undruggable” proteins: from drug discovery to clinical trials (2023) · cites this paper as [107]
In the citing paper
“Activated EGFR induces EGFR-mediated pro-survival and anti-apoptotic signals through downstream targets such as extracellular-signal-regulated kinase (ERK)/mitogen-activated protein kinase (MAPK) and phosphatidylinositol-3-kinases (PI3K)/protein kinase B (AKT) [10, 11].”
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Cites
Lynch, T. J., Bell, D. W., Sordella, R., Gurubhagavatula, S., Okimoto, R. A., Brannigan, B. W., Harris, P. L., Haserlat, S. M., Supko, J. G., Haluska, F. G., et al. (2004) · New England Journal of Medicine · doi:10.1056/nejmoa040938 · Cited by 11,486
Self-citationEGFR Mutations in Lung Cancer: Correlation with Clinical Response to Gefitinib Therapy
Paez, J. G., Jänne, P. A., Lee, J. C., Tracy, S., Greulich, H., Gabriel, S., Herman, P., Kaye, F. J., Lindeman, N., Boggon, T. J., et al. (2004) · Science · doi:10.1126/science.1099314 · Cited by 9,368
Erlotinib in Previously Treated Non–Small-Cell Lung Cancer
Shepherd, F. A., Rodrigues Pereira, J., Ciuleanu, T., Tan, E. H., Hirsh, V., Thongprasert, S., Campos, D., Maoleekoonpiroj, S., Smylie, M., Martins, R., et al. (2005) · New England Journal of Medicine · doi:10.1056/nejmoa050753 · Cited by 5,419
Pao, W., Miller, V., Zakowski, M., Doherty, J., Politi, K., Sarkaria, I., Singh, B., Heelan, R., Rusch, V., Fulton, L., et al. (2004) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0405220101 · Cited by 4,338
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
Effects of a selective inhibitor of the Abl tyrosine kinase on the growth of Bcr–Abl positive cells
Druker, B. J., Tamura, S., Buchdunger, E., Ohno-Jones, S., Segal, G. M., Fanning, S., Zimmermann, J., & Lydon, N. (1996) · Nature Medicine · doi:10.1038/nm0596-561 · Cited by 3,652
Pao, W., Miller, V. A., Politi, K. A., Riely, G. J., Somwar, R., Zakowski, M. F., Kris, M. G., & Varmus, H. (2005) · PLoS Medicine · doi:10.1371/journal.pmed.0020073 · Cited by 3,527
ERBB receptors and cancer: the complexity of targeted inhibitors
Hynes, N. E., & Lane, H. A. (2005) · Nature reviews. Cancer · doi:10.1038/nrc1609 · Cited by 3,379
The Consensus Coding Sequences of Human Breast and Colorectal Cancers
Sjöblom, T., Jones, S., Wood, L. D., Parsons, D. W., Lin, J., Barber, T. D., Mandelker, D. L., Leary, R. J., Ptak, J., Silliman, N., et al. (2006) · Science · doi:10.1126/science.1133427 · Cited by 3,161
Clinical Resistance to STI-571 Cancer Therapy Caused by BCR-ABL Gene Mutation or Amplification
Gorre, M. E., Mohammed, M., Ellwood, K., Hsu, N., Paquette, R., Rao, P. N., & Sawyers, C. L. (2001) · Science · doi:10.1126/science.1062538 · Cited by 3,104
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2 of the 182 references couldn’t be matched to a known paper.
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Items 1,001–1,006 of 1,006
Genetic Modification of the Lung Directed Toward Treatment of Human Disease
Sondhi, D., Stiles, K. M., De, B. P., & Crystal, R. G. (2017) · Human Gene Therapy · doi:10.1089/hum.2016.152 · Cited by 36
Abdallah, M., Marzocco, S., Adesso, S., Zarrouk, M., & Guerfel, M. (2018) · Acta Histochemica · doi:10.1016/j.acthis.2017.10.005 · Cited by 35
Murakami, H., Nokihara, H., Hayashi, H., Seto, T., Park, K., Azuma, K., Tsai, C., Yang, J. C., Nishio, M., Kim, S., et al. (2018) · Cancer Science · doi:10.1111/cas.13724 · Cited by 17
Wheler, J., Falchook, G., Tsimberidou, A. M., Hong, D., Naing, A., Piha-Paul, S., Chen, S. S., Heymach, J., Fu, S., Stephen, B., et al. (2013) · Oncotarget · doi:10.18632/oncotarget.1028 · Cited by 17
Zheng, J., Shen, L., Jiang, N., Zhu, Y., Wu, L., Cao, H., Sun, W., Zhou, J., & Zhou, J. (2020) · Clinical Lung Cancer · doi:10.1016/j.cllc.2020.07.001 · Cited by 6
Eck, M. J., & Hahn, W. C. (2012) · Cell · doi:10.1016/j.cell.2012.04.015 · Cited by 5
Metadata
- Authors
- Sharma, S. V., Bell, D. W., Settleman, J., & Haber, D. A.
- Affiliations
- Harvard University (US)
- National Institutes of Health (US)
- Corresponding author
- Haber, Daniel A.
- Venue
- Nature Reviews Cancer
- Published
- 2007-03
- Volume
- 7
- Issue
- 3
- Pages
- 169-181
- ISSN
- 1474-175X (ISSN-L)
- 1474-1768
- OpenAlex
- W1967394241
- Cited by
- 3,170
- References
- 182
- Citations by year
- 2026: 85 · 2025: 130 · 2024: 131 · 2023: 168 · 2022: 186 · 2021: 181 · 2020: 175 · 2019: 154 · 2018: 209 · 2017: 213 · 2016: 186 · 2015: 205 · 2014: 191 · 2013: 206 · 2012: 189
- FWCI
- 21.12
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature reviews. Cancer (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Treatments and Mutations
- Health Sciences › Medicine › Oncology › HER2/EGFR in Cancer Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Keywords
- epidermal growth factor receptor, EGFR mutation, lung cancer, tyrosine kinase inhibitors, drug resistance, oncogene addiction, apoptosis, genetic heterogeneity, targeted cancer therapy, epithelial tumors
- MeSH terms
- Animals, Antineoplastic Agents, Carcinoma, Non-Small-Cell Lung, Humans, Lung Neoplasms, Mutation, Drug Resistance, Neoplasm, Protein Kinase Inhibitors, ErbB Receptors
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