Cited by 110Lung Cancer Treatments and MutationsHER2/EGFR in Cancer ResearchCancer Genomics and Diagnostics

The DOI matches its Crossref record; 83 of the 86 references it cites were found in a registry or an index.

Uncommon Epidermal Growth Factor Receptor mutations in non-small cell lung cancer and their mechanisms of EGFR tyrosine kinase inhibitors sensitivity and resistance

Abstract

Therapy targeted against the epidermal growth factor receptor (EGFR) has demonstrated dramatic tumor responses and favorable clinical outcomes in a select group of non-small cell lung cancer (NSCLC) patients whose tumors harbor EGFR activating mutations. The best characterized of the mutations conferring sensitivity to EGFR tyrosine kinase inhibitors (TKIs) are deletions in exon 19 and a point mutation in exon 21 (L858R). Likewise, the most common mutation that confers resistance is the T790M point mutation. However several other mutations have been reported and several have been characterized as regards their role in sensitivity or resistance to EGFR TKIs. Resistance to the EGFR TKIs erlotinib and gefitinib, and the newer irreversible EGFR TKIs is a problem of fundamental importance. Recognition of the presence and significance of specific EGFR mutations is important for appropriate therapeutic implementation of EGFR TKIs and research and development of mutation-specific inhibitors. We summarize the literature and present an overview of the subject of less common EGFR mutations and their clinical significance, with an emphasis on EGFR TKI sensitivity or resistance.

Overview

Integrity signals

Registry

Crossref · 10.1016/j.lungcan.2013.01.018

Cites

83 of 83 references verified0 citation errors · 0 not checkable

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Citations

Cites

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3 of the 86 references couldn’t be matched to a known paper.

Research works printed but not linked: 2

  1. Shih, 2011, Activity of BIBW 2992, an irreversible EGFR/HER1 TKI, in lung adenocarcinoma patients harboring less common EGFR mutations, Ann Oncol, 21, 415
  2. Horn, 2011, Activity and tolerability of combined EGFR targeting wih afatinib (BIBW 2992) and cetuximab in T790M+ NSCLC patients. J Thorac Oncol, 6, S39

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Metadata

Authors
Massarelli, E., Johnson, F. M., Erickson, H. S., Wistuba, I. I., & Papadimitrakopoulou, V.
Affiliations
The University of Texas MD Anderson Cancer Center (US)
Corresponding author
Papadimitrakopoulou, Vassiliki
Venue
Lung Cancer
Publisher
Elsevier BV
Published
2013-06
Volume
80
Issue
3
Pages
235-241
ISSN
0169-5002 (ISSN-L)
OpenAlex
W2014993624
Cited by
110
References
86
Citations by year
2026: 2 · 2025: 5 · 2024: 9 · 2023: 5 · 2022: 16 · 2021: 8 · 2020: 11 · 2019: 9 · 2018: 8 · 2017: 7 · 2016: 8 · 2015: 8 · 2014: 10 · 2013: 4
FWCI
1.56
Type
journal article
Language
en
Open access
closed
Locations
  • Lung Cancer (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
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
Keywords
EGFR mutation, non-small cell lung cancer, EGFR tyrosine kinase inhibitors, drug resistance, erlotinib, gefitinib, exon 19 deletion, L858R mutation, T790M mutation, targeted therapy
MeSH terms
Antineoplastic Agents, Carcinoma, Non-Small-Cell Lung, Exons, Humans, Point Mutation, Drug Resistance, Neoplasm, Protein Kinase Inhibitors, ErbB Receptors

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