Cited by 171Lung Cancer Treatments and MutationsHER2/EGFR in Cancer ResearchLung Cancer Diagnosis and Treatment

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Effects of Erlotinib in EGFR Mutated Non-Small Cell Lung Cancers with Resistance to Gefitinib

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Costa, Daniel B., Nguyen, Kim-Son H., Cho, Byoung C., Sequist, Lecia V., Jackman, David M., Riely, Gregory J., Yeap, Beow Y., Halmos, Balázs, Kim, Joo H., Jänne, Pasi A., Huberman, Mark S., Pao, William, Tenen, Daniel G., Kobayashi, Susumu·2008·Clinical Cancer Research

DOI 10.1158/1078-0432.ccr-08-1455PMC PMC2596582

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Abstract

Purpose: Most lung cancers with activating epidermal growth factor receptor (EGFR) mutations respond to gefitinib; however, resistance to this tyrosine kinase inhibitor (TKI) invariably ensues. The T790M mutation occurs in 50% and MET amplification in 20% of TKI-resistant tumors. Other secondary mutations (D761Y and L747S) are rare. Our goal was to determine the effects of erlotinib 150 mg/d in EGFR mutated patients resistant to gefitinib 250 mg/d, because the EGFR TKI erlotinib is given at a higher biologically active dose than gefitinib. Experimental Design: Retrospective review of 18 EGFR mutated (exon 19 deletions, L858R, and L861Q) patients that were given gefitinib and subsequently erlotinib. Seven patients had tumor resampling after TKI therapy and were analyzed for secondary EGFR mutations and MET amplification. Results: Most patients (14 of 18) responded to gefitinib with median progression-free survival of 11 months (95% confidence interval, 4-16). After gefitinib resistance (de novo or acquired), 78% (14 of 18) of these patients displayed progressive disease while on erlotinib with progression-free survival of 2 months (95% confidence interval, 2-3). Six of 7 resampled patients acquired the T790M mutation, and 0 of 3 had MET amplification. Only 1 gefitinib-resistant patient with the acquired L858R-L747S EGFR, which in vitro is sensitive to achievable serum concentrations of erlotinib 150 mg/d, achieved a partial response to erlotinib. Conclusions: In EGFR mutated tumors resistant to gefitinib 250 mg/d, a switch to erlotinib 150 mg/d does not lead to responses in most patients. These findings are consistent with preclinical models, because the common mechanisms of TKI resistance (T790M and MET amplification) in vitro are not inhibited by clinically achievable doses of gefitinib or erlotinib. Alternative strategies to overcome TKI resistance must be evaluated.

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Rôle des calpaïnes extracellulaires dans la progression des adénocarcinomes lépidiques
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BindingDB Entry 50022342: The mystery of titan hunter: Rationalized striking of the MAPK pathway via Newly synthesized 6-Indolylpyridone-3-Carbonitrile derivatives.
BindingDB (2025) · UC San Diego · doi:10.7270/q2jd52jm

Authors: Costa, D. B., Nguyen, K.-S. H., Cho, B. C., Sequist, L. V., Jackman, D. M., Riely, G. J., Yeap, B. Y., Halmos, B., Kim, J. H., Jänne, P. A., Huberman, M. S., Pao, W., Tenen, D. G., & Kobayashi, S.
Affiliations: Beth Israel Deaconess Medical Center (US)
Yonsei University (KR)
Massachusetts General Hospital (US)
Harvard University (US)
Memorial Sloan Kettering Cancer Center (US)
6Case Western Reserve University, Cleveland, Ohio
3Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts;
ORCID: Costa, Daniel B.
Cho, Byoung C.
Sequist, Lecia V.
Riely, Gregory J.
Yeap, Beow Y.
Pao, William
Tenen, Daniel G.
Kobayashi, Susumu
Venue: Clinical Cancer Research
Publisher: American Association for Cancer Research (AACR)
Published: 2008-11-01
Volume: 14
Issue: 21
Pages: 7060-7067
ISSN: 1078-0432 (ISSN-L)
1557-3265
DOI: 10.1158/1078-0432.ccr-08-1455
PMC: PMC2596582
OpenAlex: W2154226624
Cited by: 171
References: 67
Citations by year: 2026: 1 · 2025: 11 · 2024: 6 · 2023: 4 · 2022: 3 · 2021: 5 · 2020: 4 · 2019: 9 · 2018: 4 · 2017: 6 · 2016: 14 · 2015: 10 · 2014: 15 · 2013: 18 · 2012: 24
FWCI: 11.32
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Clinical Cancer Research (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: Pfizer
AstraZeneca
National Institutes of Health
Genentech
National Cancer Institute (2PA50-CA09057806, R01CA114465, P50CA090578, K99CA126026, P20CA090578)
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 › Pulmonary and Respiratory Medicine › Lung Cancer Diagnosis and Treatment
Keywords: erlotinib, gefitinib, EGFR mutation, non-small cell lung cancer, tyrosine kinase inhibitor resistance, T790M mutation, MET amplification, exon 19 deletion, L858R, progression-free survival, drug dose comparison
MeSH terms: Erlotinib Hydrochloride, Gefitinib, Adenocarcinoma, Adult, Aged, Aged, 80 and over, Antineoplastic Agents, Carcinoma, Non-Small-Cell Lung, Female, Humans, Lung Neoplasms, Male, Middle Aged, Mutation, Quinazolines, Drug Resistance, Neoplasm, Protein Kinase Inhibitors, ErbB Receptors

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Effects of Erlotinib in EGFR Mutated Non-Small Cell Lung Cancers with Resistance to Gefitinib

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