The DOI matches its Crossref record; 25 of the 25 references it cites were found in a registry or an index.
EGFR Mutations in Lung Cancer: Correlation with Clinical Response to Gefitinib Therapy
Abstract
Receptor tyrosine kinase genes were sequenced in non-small cell lung cancer (NSCLC) and matched normal tissue. Somatic mutations of the epidermal growth factor receptor gene EGFR were found in 15of 58 unselected tumors from Japan and 1 of 61 from the United States. Treatment with the EGFR kinase inhibitor gefitinib (Iressa) causes tumor regression in some patients with NSCLC, more frequently in Japan. EGFR mutations were found in additional lung cancer samples from U.S. patients who responded to gefitinib therapy and in a lung adenocarcinoma cell line that was hypersensitive to growth inhibition by gefitinib, but not in gefitinib-insensitive tumors or cell lines. These results suggest that EGFR mutations may predict sensitivity to gefitinib.
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In the citing paper
“Afterwards, studies revealed that the reduced sensitivity to gefitinib or erlotinib in NSCLC was linked to EGFR-specific activating mutations.112–116”
From Recent advances in targeting the “undruggable” proteins: from drug discovery to clinical trials (2023) · cites this paper as [113]
In the citing paper
“The two most common EGFR-activating mutations are small in-frame deletions in exon 19 (particularly E746-A750del) and amino acid substitution in exon 21 (leucine to arginine at codon 858 (L858R)), which collectively account for >90% of known activating EGFR mutations.2 3”
From Mechanisms of resistance to EGFR-targeted drugs: lung cancer (2016) · cites this paper as [3]
In the citing paper
“Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) are effective clinical therapies for EGFR mutant advanced non small cell lung cancer (NSCLC) patients (1–4).”
From EGFR Mutations and Resistance to Irreversible Pyrimidine-Based EGFR Inhibitors (2015) · cites this paper as [2]
In the citing paper
“In 2004 two different groups simultaneously identified the presence of somatic mutations in the tyrosine kinase domain of the EGFR in a small group of patients with NSCLC responding to the EGFR tyrosine kinase inhibitor (TKI) Gefitinib [5, 6].”
From A decade of EGFR inhibition in EGFR-mutated non small cell lung cancer (NSCLC): Old successes and future perspectives (2015) · cites this paper as [5]
In the citing paper
“Fortunately, common mutations (i.e. exon 19 deletions [Del19] and L858R mutation in exon 21) are associated with sensitivity to EGFR tyrosine kinase inhibitors (TKI).3, 4”
From Not all epidermal growth factor receptor mutations in lung cancer are created equal: Perspectives for individualized treatment strategy (2016) · cites this paper as [4]
In the citing paper
“During clinical development in the early 2000s, the reversible, first-generation EGFR inhibitors gefitinib and erlotinib (Fig. 2a) were discovered to be effective against tumours harbouring somatic activating mutations in EGFR, either deletions in exon 19 or the L858R point mutation, which occur in 10–30% of patients with NSCLC31–33.”
From Advances in covalent drug discovery (2022) · cites this paper as [32]
In the citing paper
“The causal role of EGFR in tumorigenesis was further solidified in 2004 when somatic, activating mutations in EGFR were discovered in a subset of non-small cell lung cancers (NSCLC) (Lynch et al., 2004; Paez et al., 2004; Pao et al., 2004) (Table 1).”
From ERBB Receptors: From Oncogene Discovery to Basic Science to Mechanism-Based Cancer Therapeutics (2014) · cites this paper as Paez et al., 2004
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Metadata
- Authors
- 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., Naoki, K., Sasaki, H., Fujii, Y., Eck, M. J., Sellers, W. R., Johnson, B. E., & Meyerson, M.
- Affiliations
- Broad Institute (US)
- Departments of Medical Oncology and Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02115, USA.
- Corresponding author
- Paez, J. Guillermo
- Lee, Jeffrey C.
- Sellers, William R.
- Johnson, Bruce E.
- Meyerson, Matthew
- ORCID
- Venue
- Science
- Published
- 2004-06-04
- Volume
- 304
- Issue
- 5676
- Pages
- 1497-1500
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W2161821474
- Cited by
- 9,368
- References
- 25
- Citations by year
- 2026: 118 · 2025: 167 · 2024: 178 · 2023: 225 · 2022: 291 · 2021: 294 · 2020: 315 · 2019: 333 · 2018: 430 · 2017: 488 · 2016: 505 · 2015: 563 · 2014: 569 · 2013: 575 · 2012: 549
- FWCI
- 513.65
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Treatments and Mutations
- Health Sciences › Medicine › Oncology › HER2/EGFR in Cancer Research
- Health Sciences › Medicine › Oncology › Lung Cancer Research Studies
- Keywords
- EGFR mutation, non-small cell lung cancer, gefitinib, EGFR tyrosine kinase inhibitors, predictive biomarkers, treatment response, lung adenocarcinoma, somatic mutations, drug sensitivity
- MeSH terms
- Gefitinib, Adenocarcinoma, Amino Acid Sequence, Antineoplastic Agents, Carcinoma, Non-Small-Cell Lung, Enzyme Inhibitors, Female, Humans, Japan, Lung Neoplasms, Male, Molecular Sequence Data, Mutation, Phosphorylation, Protein Conformation, Quinazolines, United States, Treatment Outcome, Sequence Deletion, Protein Structure, Tertiary, Genes, erbB-1, Controlled Clinical Trials as Topic, Amino Acid Substitution, Mutation, Missense, Amino Acid Motifs, Cell Line, Tumor, ErbB Receptors
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