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Gefitinib or Carboplatin–Paclitaxel in Pulmonary Adenocarcinoma
Open accessAbstract
BACKGROUND: Previous, uncontrolled studies have suggested that first-line treatment with gefitinib would be efficacious in selected patients with non-small-cell lung cancer. METHODS: In this phase 3, open-label study, we randomly assigned previously untreated patients in East Asia who had advanced pulmonary adenocarcinoma and who were nonsmokers or former light smokers to receive gefitinib (250 mg per day) (609 patients) or carboplatin (at a dose calculated to produce an area under the curve of 5 or 6 mg per milliliter per minute) plus paclitaxel (200 mg per square meter of body-surface area) (608 patients). The primary end point was progression-free survival. RESULTS: The 12-month rates of progression-free survival were 24.9% with gefitinib and 6.7% with carboplatin-paclitaxel. The study met its primary objective of showing the noninferiority of gefitinib and also showed its superiority, as compared with carboplatin-paclitaxel, with respect to progression-free survival in the intention-to-treat population (hazard ratio for progression or death, 0.74; 95% confidence interval [CI], 0.65 to 0.85; P<0.001). In the subgroup of 261 patients who were positive for the epidermal growth factor receptor gene (EGFR) mutation, progression-free survival was significantly longer among those who received gefitinib than among those who received carboplatin-paclitaxel (hazard ratio for progression or death, 0.48; 95% CI, 0.36 to 0.64; P<0.001), whereas in the subgroup of 176 patients who were negative for the mutation, progression-free survival was significantly longer among those who received carboplatin-paclitaxel (hazard ratio for progression or death with gefitinib, 2.85; 95% CI, 2.05 to 3.98; P<0.001). The most common adverse events were rash or acne (in 66.2% of patients) and diarrhea (46.6%) in the gefitinib group and neurotoxic effects (69.9%), neutropenia (67.1%), and alopecia (58.4%) in the carboplatin-paclitaxel group. CONCLUSIONS: Gefitinib is superior to carboplatin-paclitaxel as an initial treatment for pulmonary adenocarcinoma among nonsmokers or former light smokers in East Asia. The presence in the tumor of a mutation of the EGFR gene is a strong predictor of a better outcome with gefitinib. (ClinicalTrials.gov number, NCT00322452.)
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In the citing paper
“have shown improved efficacy and tolerability compared with chemotherapy in numerous phase III trials”
From Afatinib for the treatment of EGFR mutation-positive NSCLC: A review of clinical findings (2020) · cites this paper as [31]
Experimental — accuracy not yet measuredIn 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 [115]
In the citing paper
“Eight randomised controlled phase III trials (table 1) have demonstrated that first-generation or second-generation EGFR-TKIs represent the best first-line treatment option in patients with advanced NSCLC whose tumours harbour EGFR mutations, when compared with chemotherapy, because they significantly improved the RR and progression-free survival (PFS).4–11”
From Mechanisms of resistance to EGFR-targeted drugs: lung cancer (2016) · cites this paper as [4]
In the citing paper
“Unfortunately, whilst patients with EGFRm+ tumors typically show good initial responses to first generation TKIs, most patients who respond to therapy ultimately develop disease progression after about 9-14 months of treatment (7-11).”
From AZD9291, an Irreversible EGFR TKI, Overcomes T790M-Mediated Resistance to EGFR Inhibitors in Lung Cancer (2014) · cites this paper as [9]
In the citing paper
“Even more variable are duration of response to targeted therapy, progression-free survival and overall survival16–26, 28–32, 35.”
From Co-occurring genomic alterations in non-small-cell lung cancer biology and therapy (2019) · cites this paper as [16]
In the citing paper
“Across clinical trials of first-line targeted therapy for oncogene-addicted subgroups of NSCLC, rates of objective response [G] typically range between 50% and 83% and complete responses [G] are rare; in addition, some patients exhibit de novo resistance16–26, 28–32, 35.”
From Co-occurring genomic alterations in non-small-cell lung cancer biology and therapy (2019) · cites this paper as [16]
In the citing paper
“The magnitude of the improvement in progression-free survival observed in the current study is similar to that observed in studies of EGFR-mutation-positive tumors treated with firstline EGFR tyrosine kinase inhibitors.[24][25][26]”
From First-Line Crizotinib versus Chemotherapy in ALK -Positive Lung Cancer (2014) · cites this paper as [24]
In the citing paper
“The presence of a sensitizing EGFR mutation usually indicates a high likelihood of response to first-generation tyrosine kinase inhibitors (TKIs), but most patients will develop resistance within 12–24 months of treatment initiation (7–9).”
In the citing paper
“EGFR exon 19 deletions and EGFR exon 21 L858R represent the vast majority of EGFR activating mutations, and are exquisitely sensitive to approved EGFR TKIs such as erlotinib, gefitinib, and afatinib”
From Diverse EGFR Exon 20 Insertions and Co-Occurring Molecular Alterations Identified by Comprehensive Genomic Profiling of NSCLC (2018) · cites this paper as [1]
In the citing paper
“acquired resistance develops after a median of 9 to 13 months [2][3][4]”
From Rociletinib in EGFR-Mutated Non–Small-Cell Lung Cancer (2015) · cites this paper as [2]
In the citing paper
“Most patients whose tumors harbor exon 19 deletions or L858R EGFR activating mutations have radiographic responses to monotherapy with the reversible adenosine triphosphate (ATP)-competitive EGFR tyrosine kinase inhibitors (TKIs) gefitinib and erlotinib 17–23 and the irreversible EGFR TKI afatinib 24.”
From Structural, Biochemical, and Clinical Characterization of Epidermal Growth Factor Receptor (EGFR) Exon 20 Insertion Mutations in Lung Cancer (2013) · cites this paper as [22]
In the citing paper
“Response rates to EGFR TKIs in patients with NSCLC with sensitizing EGFR mutations (exon 19 deletions or L858R) are approximately 60% to 80%, 3,5”
From Osimertinib for Patients With Non–Small-Cell Lung Cancer Harboring Uncommon EGFR Mutations: A Multicenter, Open-Label, Phase II Trial (KCSG-LU15-09) (2020) · cites this paper as [5]
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 [1]
In the citing paper
“Several randomized clinical trials have demonstrated that EGFR TKIs are more effective, as measured by response rate (RR) and progression free survival (PFS), than chemotherapy when used as initial systemic treatment for advanced EGFR mutant NSCLC (1, 4–9).”
From EGFR Mutations and Resistance to Irreversible Pyrimidine-Based EGFR Inhibitors (2015) · cites this paper as [1]
In the citing paper
“Gefitinib was the first EGFR TKI receiving regulatory approval for EGFR-mutated NSCLC patients after the publication of the results of the IPASS (Iressa Pan-Asia Study) trial, reporting a significant advantage in terms of PFS and ORR for first-line Gefitinib versus Carboplatin/Paclitaxel [63].”
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 [63]
In the citing paper
“Randomized phase III trials have demonstrated the superiority of these TKI, in terms of progression free survival (PFS), to conventional chemotherapy in patients with lung cancers harboring EGFR mutations.5, 6, 11”
From Not all epidermal growth factor receptor mutations in lung cancer are created equal: Perspectives for individualized treatment strategy (2016) · cites this paper as [11]
In the citing paper
“Despite high tumor response rates with first-line EGFR-TKIs, disease progresses in a majority of patients after 9 to 13 months of treatment.5–12”
From Osimertinib or Platinum–Pemetrexed in EGFR T790M–Positive Lung Cancer (2017) · cites this paper as [12]
In the citing paper
“Resistance to conventional EGFR-TKIs develops after a median of 10 to 12 months and is most commonly mediated by an acquired mutation, T790M1-5.”
From Association Between Plasma Genotyping and Outcomes of Treatment With Osimertinib (AZD9291) in Advanced Non–Small-Cell Lung Cancer (2016) · cites this paper as [2]
In the citing paper
“As a classic oncogene-driven solid tumor, EGFR mutation-positive NSCLC has a unique disease course typified by high response rates to tyrosine kinase inhibitors (TKIs).6”
In the citing paper
“Several studies have consistently demonstrated that the EGFR TKIs (gefitinib, erlotinib and afatinib) produce higher RRs, longer PFS and improve QoL compared with standard platinum-based doublet chemotherapy in patients with good PS (PS 0-2), whose tumour harbours an activating (sensitising) EGFR mutation [105-112].”
From Metastatic non-small-cell lung cancer: ESMO Clinical Practice Guidelines for diagnosis, treatment and follow-up (2016) · cites this paper as [105]
In the citing paper
“A statistically significant PFS was found for all patients in the trial treated with gefitinib, including those whose tumors were EGFR mutation positive.61”
From Systemic Therapy for Stage IV Non–Small-Cell Lung Cancer: American Society of Clinical Oncology Clinical Practice Guideline Update (2015) · cites this paper as [61]
In the citing paper
“In the IPASS trial comparing gefitinib with carboplatin plus paclitaxel, in the subgroup of patients with unknown EGFR mutation status, there were statistically significantly longer PFS and higher response rates.61”
From Systemic Therapy for Stage IV Non–Small-Cell Lung Cancer: American Society of Clinical Oncology Clinical Practice Guideline Update (2015) · cites this paper as [61]
In the citing paper
“It is now well established that lung cancers harboring these EGFR mutations are highly responsive to single-agent EGFR inhibitors with RECIST response rates of ~55%–75% (Mok et al., 2009; Rosell et al., 2012; Sequist et al., 2013b).”
From ERBB Receptors: From Oncogene Discovery to Basic Science to Mechanism-Based Cancer Therapeutics (2014) · cites this paper as Mok et al., 2009
In the citing paper
“In clinical trials, the incidence of all-grade liver injury due to different smallmolecule targeted drugs such as tyrosine kinase inhibitors is reportedly 5-55% [144-149].”
From Chinese guideline for the diagnosis and treatment of drug-induced liver injury: an update (2024) · cites this paper as [144]
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Metadata
- Authors
- Mok, T. S., Wu, Y.-L., Thongprasert, S., Yang, C.-H., Chu, D.-T., Saijo, N., Sunpaweravong, P., Han, B., Margono, B., Ichinose, Y., Nishiwaki, Y., Ohe, Y., Yang, J.-J., Chewaskulyong, B., Jiang, H., Duffield, E. L., Watkins, C. L., Armour, A. A., & Fukuoka, M.
- Affiliations
- Chinese University of Hong Kong (HK)
- Maharaj Nakorn Chiang Mai Hospital (TH)
- National Taiwan University Hospital (TW)
- Chinese Academy of Medical Sciences & Peking Union Medical College (CN)
- National Cancer Center Hospital East (JP)
- Prince of Songkla University (TH)
- Shanghai Chest Hospital (CN)
- Rumah Sakit Dokter Soetomo (ID)
- National Hospital Organization Kyushu Cancer Center (JP)
- National Cancer Center Hospital (JP)
- Guangdong General Hospital (CN)
- AstraZeneca (Japan) (JP)
- AstraZeneca (United Kingdom) (GB)
- Kindai University Hospital (JP)
- ORCID
- Venue
- New England Journal of Medicine
- Publisher
- Massachusetts Medical Society
- Published
- 2009-09-03
- Volume
- 361
- Issue
- 10
- Pages
- 947-957
- ISSN
- 0028-4793 (ISSN-L)
- 1533-4406
- OpenAlex
- W2166084034
- Cited by
- 8,261
- References
- 32
- Citations by year
- 2026: 188 · 2025: 268 · 2024: 238 · 2023: 317 · 2022: 373 · 2021: 408 · 2020: 474 · 2019: 529 · 2018: 545 · 2017: 615 · 2016: 601 · 2015: 693 · 2014: 674 · 2013: 656 · 2012: 623
- FWCI
- 470.13
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- New England Journal of Medicine (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Treatments and Mutations
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Diagnosis and Treatment
- Health Sciences › Medicine › Oncology › Lung Cancer Research Studies
- Keywords
- gefitinib, carboplatin, paclitaxel, lung adenocarcinoma, non-small cell lung cancer, EGFR mutation, progression-free survival, first-line therapy, non-inferiority, EGFR tyrosine kinase inhibitors, East Asia, non-smokers, light smokers, neurotoxicity, neutropenia, hair loss
- MeSH terms
- Gefitinib, Adenocarcinoma, Adult, Aged, Aged, 80 and over, Antineoplastic Agents, Antineoplastic Combined Chemotherapy Protocols, Carcinoma, Non-Small-Cell Lung, Female, Humans, Lung Neoplasms, Male, Middle Aged, Mutation, Quinazolines, Proportional Hazards Models, Carboplatin, Paclitaxel, Disease-Free Survival, Protein Kinase Inhibitors, Kaplan-Meier Estimate, ErbB Receptors
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