The DOI matches its Crossref record; 23 of the 23 references it cites were found in a registry or an index.
Erlotinib versus standard chemotherapy as first-line treatment for European patients with advanced EGFR mutation-positive non-small-cell lung cancer (EURTAC): a multicentre, open-label, randomised phase 3 trial
Open accessAbstract
Background Erlotinib has been shown to improve progression-free survival compared with chemotherapy when given as first-line treatment for Asian patients with non-small-cell lung cancer (NSCLC) with activating EGFR mutations. We aimed to assess the safety and efficacy of erlotinib compared with standard chemotherapy for first-line treatment of European patients with advanced EGFR-mutation positive NSCLC.Methods We undertook the open-label, randomised phase 3 EURTAC trial at 42 hospitals in France, Italy, and Spain. Eligible participants were adults (> 18 years) with NSCLC and EGFR mutations (exon 19 deletion or L858R mutation in exon 21) with no history of chemotherapy for metastatic disease (neoadjuvant or adjuvant chemotherapy ending ≥ 6 months before study entry was allowed). We randomly allocated participants (1:1) according to a computer-generated allocation schedule to receive oral erlotinib 150 mg per day or 3 week cycles of standard intravenous chemotherapy of cisplatin 75 mg/m(2) on day 1 plus docetaxel (75 mg/m(2) on day 1) or gemcitabine (1250 mg/m(2) on days 1 and 8). Carboplatin (AUC 6 with docetaxel 75 mg/m(2) or AUC 5 with gemcitabine 1000 mg/m(2)) was allowed in patients unable to have cisplatin. Patients were stratified by EGFR mutation type and Eastern Cooperative Oncology Group performance status (0 vs 1 vs 2). The primary endpoint was progression-free survival (PFS) in the intention-to-treat population. We assessed safety in all patients who received study drug (≥ 1 dose). This study is registered with ClinicalTrials.gov, number NCT00446225.Findings Between Feb 15, 2007, and Jan 4, 2011, 174 patients with EGFR mutations were enrolled. One patient received treatment before randomisation and was thus withdrawn from the study; of the remaining patients, 86 were randomly assigned to receive erlotinib and 87 to receive standard chemotherapy. The preplanned interim analysis showed that the study met its primary endpoint; enrolment was halted, and full evaluation of the results was recommended. At data cutoff (Jan 26, 2011), median PFS was 9·7 months (95% CI 8·4-12·3) in the erlotinib group, compared with 5·2 months (4·5-5·8) in the standard chemotherapy group (hazard ratio 0·37, 95% CI 0·25-0·54; p < 0·0001). Main grade 3 or 4 toxicities were rash (11 [13%] of 84 patients given erlotinib vs none of 82 patients in the chemotherapy group), neutropenia (none vs 18 [22%]), anaemia (one [1%] vs three [4%]), and increased amino-transferase concentrations (two [2%] vs 0). Five (6%) patients on erlotinib had treatment-related severe adverse events compared with 16 patients (20%) on chemotherapy. One patient in the erlotinib group and two in the standard chemotherapy group died from treatment-related causes.Interpretation Our findings strengthen the rationale for routine baseline tissue-based assessment of EGFR mutations in patients with NSCLC and for treatment of mutation-positive patients with EGFR tyrosine-kinase inhibitors.Funding Spanish Lung Cancer Group, Roche Farma, Hoffmann-La Roche, and Red Temática de Investigacion Cooperativa en Cancer.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
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 [32]
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 [147]
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 [116]
In the citing paper
“The third-generation EGFR-TKIs include the WZ4002, CO-1686, AZD9291 and HM61713 inhibitors, which have demonstrated tumour responses in >50% of patients with the EGFR T790M mutation.8–12”
From Mechanisms of resistance to EGFR-targeted drugs: lung cancer (2016) · cites this paper as [9]
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 [9]
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 [10]
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 [18]
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 [18]
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 [25]
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 [2]
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 [3]
In the citing paper
“Targeted therapies are approved for patients with ‘classical’ mutations and a small number of other mutations4–6.”
From Structure-based classification predicts drug response in EGFR-mutant NSCLC (2021) · cites this paper as [4]
In the citing paper
“Patients with classical EGFR mutations (L858R or exon 19 deletions (Ex19del)) show marked improvements in clinical outcomes when treated with first-, second- or third-generation tyrosine kinase inhibitors (TKIs)4–6,11.”
From Structure-based classification predicts drug response in EGFR-mutant NSCLC (2021) · cites this paper as [4]
In the citing paper
“One potential limitation of the current diagnostic approach of testing only for common exon 19 and 21 mutations, as was done in the EURTAC or OPTIMAL studies, 4,5 is that such an approach might miss identifying a number of patients who could have some benefit from EGFR TKI treatment.”
From Examining Treatment Outcomes with Erlotinib in Patients with Advanced Non–Small Cell Lung Cancer Whose Tumors Harbor Uncommon EGFR Mutations (2016) · cites this paper as [5]
In the citing paper
“a strikingly long survival compared to median OS of 19–28 months with first- or second-generation EGFR TKIs[17–19].”
From Landscape of EGFR-Dependent and -Independent Resistance Mechanisms to Osimertinib and Continuation Therapy Beyond Progression in EGFR -Mutant NSCLC (2018) · cites this paper as [19]
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 [4]
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 [4]
In the citing paper
“The extension of approval of Erlotinib for patients harboring EGFR mutations, in addition to the previous indication for unselected patients with NSCLC after at least one chemotherapeutic line, was obtained after the publication of two large phase III trials conducted in Asia [65] and Europe [66], providing the definitive demonstration of superiority of an EGFR TKI over standard first-line”
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 [66]
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 [8]
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 [7]
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 [3]
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 [112]
In the citing paper
“In one small study, there was a PFS benefit with erlotinib (9.7 v 5.2 months; HR, 0.37; 95% CI, 0.25 to 0.54; P < .001); OS had not been reached by the time of publication.29”
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 [29]
In the citing paper
“Since the publication of the ASCO 2009 guideline and the ASCO EGFR provisional clinical opinion,59 results from seven trials of first-line EGFR TKIs for patients with EGFR mutations have been published.11,13,29,31,34,36,40”
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 [29]
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 Rosell et al., 2012
Citations
Cites
New Guidelines to Evaluate the Response to Treatment in Solid Tumors
Therasse, P., Arbuck, S. G., Eisenhauer, E. A., Wanders, J., Kaplan, R. S., Rubinstein, L., Verweij, J., Van Glabbeke, M., van Oosterom, A. T., Christian, M. C., et al. (2000) · JNCI: Journal of the National Cancer Institute · doi:10.1093/jnci/92.3.205 · Cited by 15,660
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
EGFR 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
Gefitinib or Carboplatin–Paclitaxel in Pulmonary Adenocarcinoma
Mok, T. S., Wu, Y.-L., Thongprasert, S., Yang, C.-H., Chu, D.-T., Saijo, N., Sunpaweravong, P., Han, B., Margono, B., Ichinose, Y., et al. (2009) · New England Journal of Medicine · doi:10.1056/nejmoa0810699 · Cited by 8,261
Gefitinib or Chemotherapy for Non–Small-Cell Lung Cancer with Mutated EGFR
Maemondo, M., Inoue, A., Kobayashi, K., Sugawara, S., Oizumi, S., Isobe, H., Gemma, A., Harada, M., Yoshizawa, H., Kinoshita, I., et al. (2010) · New England Journal of Medicine · doi:10.1056/nejmoa0909530 · Cited by 5,525
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
Mitsudomi, T., Morita, S., Yatabe, Y., Negoro, S., Okamoto, I., Tsurutani, J., Seto, T., Satouchi, M., Tada, H., Hirashima, T., et al. (2010) · The Lancet Oncology · doi:10.1016/s1470-2045(09)70364-x · Cited by 4,090
Zhou, C., Wu, Y.-L., Chen, G., Feng, J., Liu, X.-Q., Wang, C., Zhang, S., Wang, J., Zhou, S., Ren, S., et al. (2011) · The Lancet Oncology · doi:10.1016/s1470-2045(11)70184-x · Cited by 4,081
Genotypic and Histological Evolution of Lung Cancers Acquiring Resistance to EGFR Inhibitors
Sequist, L. V., Waltman, B. A., Dias-Santagata, D., Digumarthy, S., Turke, A. B., Fidias, P., Bergethon, K., Shaw, A. T., Gettinger, S., Cosper, A. K., et al. (2011) · Science Translational Medicine · doi:10.1126/scitranslmed.3002003 · Cited by 3,499
Screening for Epidermal Growth Factor Receptor Mutations in Lung Cancer
Rosell, R., Moran, T., Queralt, C., Porta, R., Cardenal, F., Camps, C., Majem, M., Lopez-Vivanco, G., Isla, D., Provencio, M., et al. (2009) · New England Journal of Medicine · doi:10.1056/nejmoa0904554 · Cited by 2,373
Self-citation
Research works printed but not linked: 1
- International Conference on Harmonization of Technical Requirements for Registration of Pharmaceuticals for Human Use (ICH). Medical Dictionary for Regulatory Activities (MedDRA) version 13.0 (accessed Aug 2, 2010).
Cited by
Sorted by citations
Items 601–700 of 1,020
George, R. F., Samir, E. M., Abdelhamed, M. N., Abdel‐Aziz, H. A., & Abbas, S. E.-S. (2018) · Bioorganic Chemistry · doi:10.1016/j.bioorg.2018.10.038 · Cited by 94
Lung cancer in young adults aged 35 years or younger: A full-scale analysis and review
Liu, B., Quan, X., Xu, C., Lv, J., Li, C., Dong, L., & Liu, M. (2019) · Journal of Cancer · doi:10.7150/jca.27490 · Cited by 94
Jiang, T., Wang, P., Zhang, J., Zhao, Y., Zhou, J., Fan, Y., Shu, Y., Liu, X., Zhang, H., He, J., et al. (2021) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-021-00751-9 · Cited by 95
Canale, M., Andrikou, K., Priano, I., Cravero, P., Pasini, L., Urbini, M., Delmonte, A., Crinò, L., Bronte, G., & Ulivi, P. (2022) · Cancers · doi:10.3390/cancers14051143 · Cited by 97
Janning, M., Sueptitz, J., Albers, C., Delpy, P., Tufman, A., Velthaus-Rusik, J.-L., Reck, M., Jung, A., Kauffmann-Guerrero, D. E., Bonzheim, I., et al. (2022) · Annals of Oncology · doi:10.1016/j.annonc.2022.02.225 · Cited by 94
Corvaja, C., Passaro, A., Attili, I., Aliaga, P. T., Spitaleri, G., Signore, E. D., & de Marinis, F. (2024) · Cancer Treatment Reviews · doi:10.1016/j.ctrv.2024.102824 · Cited by 94
Pan, C.-X., Zhang, H., Tepper, C. G., Lin, T., Davis, R. R., Keck, J., Ghosh, P., Gill, P. S., Airhart, S. D., Bult, C., et al. (2015) · PLoS ONE · doi:10.1371/journal.pone.0134346 · Cited by 94
Köhler, J., & Schüler, M. (2013) · Oncology Research and Treatment · doi:10.1159/000354627 · Cited by 93
Chen, H., Yao, W., Chu, Q., Han, R., Wang, Y., Sun, J., Wang, D., Wang, Y., Cao, M., & He, Y. (2015) · Cancer Letters · doi:10.1016/j.canlet.2015.08.024 · Cited by 93
Wu, Y.-L. L. C., Sequist, L. V. D., Hu, C., Feng, J., Lü, S., Huang, Y., Li, W., Hou, M., Schüler, M., Mok, T. S. K., et al. (2016) · British Journal of Cancer · doi:10.1038/bjc.2016.420 · Cited by 93
Passiglia, F., Rizzo, S., Maïo, M. D., Galvano, A., Badalamenti, G., Listì, A., Gulotta, L., Castiglia, M., Fulfaro, F., Bazan, V., et al. (2018) · Scientific Reports · doi:10.1038/s41598-018-30780-4 · Cited by 93
Friedlaender, A., Banna, G. L., Malapelle, U., Pisapia, P., & Addeo, A. (2019) · Frontiers in Oncology · doi:10.3389/fonc.2019.00166 · Cited by 93
Molecular Mechanisms Underlying Autophagy-Mediated Treatment Resistance in Cancer
Ho, C. J., & Gorski, S. M. (2019) · Cancers · doi:10.3390/cancers11111775 · Cited by 93
Xu, J., Jin, B., Chu, T., Dong, X., Yang, H., Zhang, Y., Wu, D., Lou, Y., Zhang, X., Wang, H., et al. (2016) · Lung Cancer · doi:10.1016/j.lungcan.2016.01.018 · Cited by 92
Prognostic and predictive biomarkers in lung cancer. A review
Thunnissen, E., der Oord, K. V., & den Bakker, M. (2014) · Archiv für Pathologische Anatomie und Physiologie und für Klinische Medicin · doi:10.1007/s00428-014-1535-4 · Cited by 92
Yoshioka, H., Shimokawa, M., Seto, T., Morita, S., Yatabe, Y., Okamoto, I., Tsurutani, J., Satouchi, M., Hirashima, T., Atagi, S., et al. (2019) · Annals of Oncology · doi:10.1093/annonc/mdz399 · Cited by 92
Reguart, N., & Remon, J. (2015) · Future Oncology · doi:10.2217/fon.15.15 · Cited by 91
Self-citationEGFR: The Paradigm of an Oncogene-Driven Lung Cancer
Riely, G. J., & Yu, H. A. (2015) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-14-3154 · Cited by 91
Ulivi, P., Chiadini, E., Dazzi, C., Dubini, A., Costantini, M., Medri, L., Puccetti, M., Capelli, L., Calistri, D., Verlicchi, A., et al. (2015) · Clinical Lung Cancer · doi:10.1016/j.cllc.2015.11.004 · Cited by 91
Translating insights into tumor evolution to clinical practice: promises and challenges
Fittall, M. W., & Loo, P. V. (2019) · Genome Medicine · doi:10.1186/s13073-019-0632-z · Cited by 91
Zhang, Y., Zeng, Y., Liu, T., Du, W., Zhu, J., Liu, Z., & Huang, J. (2019) · Respiratory Research · doi:10.1186/s12931-019-1137-4 · Cited by 92
Liu, H., Zhang, B., & Sun, Z. (2020) · 癌症：英文版 · doi:10.1002/cac2.12005 · Cited by 91
Nair, J. K. R., Saeed, U. A., McDougall, C. C., Sabri, A., Kovacina, B., Raidu, B. V. S., Khokhar, R. A., Probst, S., Hirsh, V., Chankowsky, J., et al. (2020) · Canadian Association of Radiologists Journal · doi:10.1177/0846537119899526 · Cited by 91
Grève, J. D., Morán, T., Graas, M.-P., Galdermans, D., Vuylsteke, P., Canon, J.-L. R., Schallier, D. C. C., Decoster, L., Teugels, E., Massey, D., et al. (2015) · Lung Cancer · doi:10.1016/j.lungcan.2015.01.013 · Cited by 91
Bauml, J. M., Mick, R., Zhang, Y., Watt, C. D., Vachani, A., Aggarwal, C., Evans, T. L., & Langer, C. J. (2013) · Lung Cancer · doi:10.1016/j.lungcan.2013.05.011 · Cited by 91
Kou, T., Kanai, M., Yamamoto, Y., Kamada, M., Nakatsui, M., Sakuma, T., Mochizuki, H., Hiroshima, A., Sugiyama, A., Nakamura, E., et al. (2017) · Cancer Science · doi:10.1111/cas.13265 · Cited by 90
Treatment of advanced squamous cell carcinoma of the lung: a review.
Derman, B. A., Mileham, K. F., Bonomi, P., Batus, M., & Fidler, M. J. (2015) · PubMed · doi:10.3978/j.issn.2218-6751.2015.06.07 · Cited by 90
Tanimoto, A., Takeuchi, S., Arai, S., Fukuda, K., Yamada, T., Roca, X., Ong, S. T., & Yano, S. (2016) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-16-2271 · Cited by 90
de Biase, D., Visani, M., Malapelle, U., Simonato, F., Cesari, V., Bellevicine, C., Pession, A., Troncone, G., Fassina, A., & Tallini, G. (2013) · PLoS ONE · doi:10.1371/journal.pone.0083607 · Cited by 89
Management and Future Directions in Non-Small Cell Lung Cancer with Known Activating Mutations
Gerber, D. E., Gandhi, L., & Costa, D. B. (2014) · American Society of Clinical Oncology Educational Book · doi:10.14694/edbook_am.2014.34.e353 · Cited by 89
Prognostic and Predictive Value of KRAS Mutations in Advanced Non-Small Cell Lung Cancer
Sun, J., Hwang, D. W., Ahn, J. S., Ahn, M., & Park, K. (2013) · PLoS ONE · doi:10.1371/journal.pone.0064816 · Cited by 89
Intraocular Metastases — A Review
Konstantinidis, L., & Damato, B. E. (2017) · Asia-Pacific Journal of Ophthalmology · doi:10.22608/apo.201712 · Cited by 89
TAS6417, A Novel EGFR Inhibitor Targeting Exon 20 Insertion Mutations
Hasako, S., Terasaka, M., Abe, N., Uno, T., Ohsawa, H., Hashimoto, A., Fujita, R., Tanaka, K., Okayama, T., Wadhwa, R., et al. (2018) · Molecular Cancer Therapeutics · doi:10.1158/1535-7163.mct-17-1206 · Cited by 88
Epidermal Growth Factor Receptor: Pathway, Therapies, and Pipeline
Goffin, J. R., & Zbuk, K. M. (2013) · Clinical Therapeutics · doi:10.1016/j.clinthera.2013.08.007 · Cited by 88
Drug Resistance to EGFR Inhibitors in Lung Cancer
Tetsu, O., Hangauer, M. J., Phuchareon, J., Eisele, D. W., & McCormick, F. P. (2016) · Chemotherapy · doi:10.1159/000443368 · Cited by 88
Banno, E., Togashi, Y., Nakamura, Y., Chiba, M., Kobayashi, Y., Hayashi, H., Terashima, M., de Velasco, M. A., Sakai, K., Fujita, Y., et al. (2016) · Cancer Science · doi:10.1111/cas.12980 · Cited by 87
PROTAC therapy as a new targeted therapy for lung cancer
Li, J. W., Zheng, G., Kaye, F. J., & Wu, L. (2023) · Molecular Therapy · doi:10.1016/j.ymthe.2022.11.011 · Cited by 87
Kim, L., & Tsao, M. (2014) · European Respiratory Journal · doi:10.1183/09031936.00197013 · Cited by 87
High‐throughput diagnostic profiling of clinically actionable gene fusions in lung cancer
Pfarr, N., Stenzinger, A., Penzel, R., Warth, A., Dienemann, H., Schirmacher, P., Weichert, W., & Endris, V. (2015) · Genes Chromosomes and Cancer · doi:10.1002/gcc.22297 · Cited by 87
Zhou, C., & Yao, L. D. (2015) · Journal of Thoracic Oncology · doi:10.1016/j.jtho.2015.10.002 · Cited by 87
Jiang, T., Min, W., Li, Y., Yue, Z., Wu, C., & Zhou, C. (2016) · Cancer Medicine · doi:10.1002/cam4.673 · Cited by 87
Masuda, C., Yanagisawa, M., Yorozu, K., Kurasawa, M., Furugaki, K., Ishikura, N., Iwai, T., Sugimoto, M., & Yamamoto, K. (2017) · International Journal of Oncology · doi:10.3892/ijo.2017.4036 · Cited by 87
Targeted Inhibitors of EGFR: Structure, Biology, Biomarkers, and Clinical Applications
Shaban, N., Kamashev, D., Emelianova, A., & Buzdin, A. A. (2023) · Cells · doi:10.3390/cells13010047 · Cited by 88
Non-Small-Cell Lung Cancer: Treatment of Late Stage Disease: Chemotherapeutics and New Frontiers
Scheff, R. J., & Schneider, B. J. (2013) · Seminars in Interventional Radiology · doi:10.1055/s-0033-1342961 · Cited by 88
ALK inhibitors: a new targeted therapy in the treatment of advanced NSCLC
Casaluce, F., Sgambato, A., Maione, P., Rossi, A., Ferrara, C., Napolitano, A., Palazzolo, G., Ciardiello, F., & Gridelli, C. (2013) · Targeted Oncology · doi:10.1007/s11523-012-0250-9 · Cited by 87
Targeted next generation sequencing of parotid gland cancer uncovers genetic heterogeneity
Grünewald, I., Vollbrecht, C., Meinrath, J., Meyer, M. F., Heukamp, L. C., Drebber, U., Quaas, A., Beutner, D., Hüttenbrink, K., Wardelmann, E., et al. (2015) · Oncotarget · doi:10.18632/oncotarget.4015 · Cited by 86
Roca, E., Gurizzan, C., Amoroso, V., Vermi, W., Ferrari, V. D., & Berruti, A. (2017) · Cancer Treatment Reviews · doi:10.1016/j.ctrv.2017.07.007 · Cited by 86
Rulli, E., Ghilotti, F., Biagioli, E. C., Porcu, L., Marabese, M., D’Incalci, M., Bellocco, R., & Torri, V. (2018) · British Journal of Cancer · doi:10.1038/s41416-018-0302-8 · Cited by 86
Cancer-associated fibroblasts in non-small cell lung cancer: Recent advances and future perspectives
Zhang, H., Jiang, H., Zhu, L., Li, J., & Ma, S. (2021) · Cancer Letters · doi:10.1016/j.canlet.2021.05.009 · Cited by 86
Deben, C., Deschoolmeester, V., Lardon, F., Rolfo, C. D., & Pauwels, P. (2015) · Critical Reviews in Oncology/Hematology · doi:10.1016/j.critrevonc.2015.11.019 · Cited by 86
Self-citationWang, Z.-F., Ren, S., Li, W., & Gao, G. (2018) · BMC Cancer · doi:10.1186/s12885-018-4075-5 · Cited by 86
Simone, C. B., Burri, S. H., & Heinzerling, J. H. (2015) · PubMed · doi:10.3978/j.issn.2218-6751.2015.10.05 · Cited by 85
Gandara, D. R., Li, T., Lara, P. N., Kelly, K. L., Riess, J. W., Redman, M. W., & Mack, P. C. (2013) · Clinical Lung Cancer · doi:10.1016/j.cllc.2013.10.001 · Cited by 85
Baek, J. H., Sun, J., Min, Y. J., Cho, E. K., Cho, B. C., Kim, J.-H., Ahn, M., & Park, K. (2014) · Lung Cancer · doi:10.1016/j.lungcan.2014.11.013 · Cited by 85
Re, M. D., Tiseo, M., Bordi, P., D’Incecco, A., Camerini, A., Petrini, I., Lucchesi, M., Inno, A., Spada, D., Vasile, E., et al. (2016) · Oncotarget · doi:10.18632/oncotarget.6957 · Cited by 85
HOTAIR , a long noncoding RNA , is a marker of abnormal cell cycle regulation in lung cancer
Liu, M., Zhang, H., Li, Y., Wang, R., Li, Y., Zhang, H., Ren, D., Liu, H., Kang, C., & Chen, J. (2018) · Cancer Science · doi:10.1111/cas.13745 · Cited by 85
Masood, A., Kancha, R. K., & Subramanian, J. (2019) · Seminars in Oncology · doi:10.1053/j.seminoncol.2019.08.004 · Cited by 86
Molecular therapeutic targets in non-small cell lung cancer
Sankar, K. N., Gadgeel, S. M., & Qin, A. (2020) · Expert Review of Anticancer Therapy · doi:10.1080/14737140.2020.1787156 · Cited by 85
Magnuson, A. M., Bruinooge, S. S., Singh, H., Wilner, K. D., Jalal, S. I., Lichtman, S. M., Kluetz, P. G., Lyman, G. H., Klepin, H. D., Fleury, M. E., et al. (2021) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-20-3868 · Cited by 85
Sheng, M., Wang, F., Zhao, Y., Li, S., Wang, X., Shou, T., Luo, Y., & Tang, W. (2015) · European Journal of Clinical Pharmacology · doi:10.1007/s00228-015-1966-0 · Cited by 85
Vallée, A., Marcq, M., Bizieux, A., Kouri, C. E., Lacroix, H., Bennouna, J., Douillard, J., & Denis, M. G. (2013) · Lung Cancer · doi:10.1016/j.lungcan.2013.08.014 · Cited by 85
Haaland, B. A., Tan, P. S., de Castro, G., & Lopes, G. D. L., Jr. (2014) · Journal of Thoracic Oncology · doi:10.1097/jto.0000000000000156 · Cited by 84
Role of circulating-tumor DNA analysis in non-small cell lung cancer
Jiang, T., Ren, S., & Zhou, C. (2015) · Lung Cancer · doi:10.1016/j.lungcan.2015.09.013 · Cited by 84
Elbatanony, R. S., Parvathaneni, V., Kulkarni, N. S., Shukla, S. K., Chauhan, G., Kunda, N. K., & Gupta, V. (2020) · Drug Delivery and Translational Research · doi:10.1007/s13346-020-00802-8 · Cited by 84
Estrada‐Bernal, A., Le, A. T., Doak, A. E., Tirunagaru, V. G., Silva, S., Bull, M. R., Smaill, J. B., Patterson, A. V., Kim, C., Liu, S. V., et al. (2020) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-20-3555 · Cited by 84
Novel therapeutic targets in non-small cell lung cancer
Alamgeer, M., Ganju, V., & Watkins, D. N. (2013) · Current Opinion in Pharmacology · doi:10.1016/j.coph.2013.03.010 · Cited by 84
Tang, Z.-H., Chen, X., Wang, Z., Chai, K., Wang, Y., Xu, X.-H., Wang, X., Lu, J., Wang, Y., Chen, X., et al. (2016) · Scientific Reports · doi:10.1038/srep26241 · Cited by 84
Mak, K. S., Gainor, J. F., Niemierko, A., Oh, K. S., Willers, H., Choi, N. C., Loeffler, J. S., Sequist, L. V., Shaw, A. T., & Shih, H. A. (2015) · Neuro-Oncology · doi:10.1093/neuonc/nou146 · Cited by 83
Therapeutic strategy for advanced EGFR mutant non-small-cell lung carcinoma
Cadranel, J. L., Ruppert, A.-M., Beau‐Faller, M., & Wislez, M. (2013) · Critical Reviews in Oncology/Hematology · doi:10.1016/j.critrevonc.2013.06.009 · Cited by 83
The Genetic Landscape of Malignant Pleural Mesothelioma: Results from Massively Parallel Sequencing
Hylebos, M., Camp, G. V., van Meerbeeck, J. P., & de Beeck, K. O. (2016) · Journal of Thoracic Oncology · doi:10.1016/j.jtho.2016.05.020 · Cited by 83
Cell-free DNA and next-generation sequencing in the service of personalized medicine for lung cancer
Bennett, C. W., Berchem, G., Kim, Y. J., & El‐Khoury, V. (2016) · Oncotarget · doi:10.18632/oncotarget.11717 · Cited by 83
Tang, H., Zhu, J., Du, W., Liu, S., Zeng, Y., Ding, Z., Zhang, Y., Wang, X., Liu, Z., & Huang, J. (2018) · Journal of Experimental & Clinical Cancer Research · doi:10.1186/s13046-018-0811-6 · Cited by 83
Recognising Lung Cancer in Primary Care
Bradley, S. H., Kennedy, M., & Neal, R. D. (2018) · Advances in Therapy · doi:10.1007/s12325-018-0843-5 · Cited by 83
Advanced-Stage Non–Small Cell Lung Cancer: Advances in Thoracic Oncology 2018
Remón, J., Ahn, M., Girard, N., Johnson, M. L., Kim, D., Lopes, G. D. L., Jr., Pillai, R. N., Solomon, B., Villacampa, G. J., & Zhou, Q. H. (2019) · Journal of Thoracic Oncology · doi:10.1016/j.jtho.2019.03.022 · Cited by 84
Re, M. D., Crucitta, S., Gianfilippo, G., Passaro, A., Petrini, I., Restante, G., Michelucci, A., Fogli, S., de Marinis, F., Porta, C., et al. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20163951 · Cited by 84
Camidge, D. R., Morgensztern, D., Heist, R. S., Barve, M. A., Vokes, E. E., Goldman, J. W., Hong, D. S., Bauer, T. M., Strickler, J. H., Angevin, E., et al. (2021) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-21-0765 · Cited by 83
Challenges in the Use of Targeted Therapies in Non–Small Cell Lung Cancer
Rivera‐Concepción, J., Uprety, D., & Adjei, A. A. (2022) · Cancer Research and Treatment · doi:10.4143/crt.2022.078 · Cited by 84
Özdemir, B. C., Gerard, C. L., & da Silva, C. E. (2022) · Endocrinology · doi:10.1210/endocr/bqac058 · Cited by 83
A predictive model for personalized therapeutic interventions in non-small cell lung cancer
Kureshi, N., Abidi, S. S. R., & Blouin, C. (2016) · IEEE Journal of Biomedical and Health Informatics · doi:10.1109/jbhi.2014.2377517 · Cited by 83
Cufí, S., Bonavia, R., Vázquez‐Martín, A., Oliveras‐Ferraros, C., Corominas-Faja, B., Cuyàs, E., Martı́n-Castillo, B., Barrajón‐Catalán, E., Visa, J., Segura‐Carretero, A., et al. (2013) · Scientific Reports · doi:10.1038/srep02459 · Cited by 83
Hyperglycemia Associated With Targeted Oncologic Treatment: Mechanisms and Management
Goldman, J. W., Mendenhall, M. A., & Rettinger, S. R. (2016) · The Oncologist · doi:10.1634/theoncologist.2015-0519 · Cited by 83
Pharmacogenomic biomarkers for personalized cancer treatment
Rodríguez‐Antona, C., & Tarón, M. (2014) · Journal of Internal Medicine · doi:10.1111/joim.12321 · Cited by 82
Molecular Targeted Drugs and Biomarkers in NSCLC, the Evolving Role of Individualized Therapy
Domvri, K., Zarogoulidis, P., Darwiche, K., Browning, R. F., Jr., Li, Q., Turner, J. F., Kioumis, I. P., Spyratos, D., Porpodis, Κ., Papaiwannou, A., et al. (2013) · Journal of Cancer · doi:10.7150/jca.7734 · Cited by 82
Quantification of mutant alleles in circulating tumor DNA can predict survival in lung cancer
Yang, X., Zhuo, M., Ye, X., Bai, H., Wang, Z., Sun, Y., Zhao, J., An, T., Duan, J., Wu, M., et al. (2016) · Oncotarget · doi:10.18632/oncotarget.8021 · Cited by 82
Matikas, A., Mistriotis, D., Georgoulias, V., & Kotsakis, A. P. (2016) · Critical Reviews in Oncology/Hematology · doi:10.1016/j.critrevonc.2016.12.005 · Cited by 82
Bylicki, O., Paleiron, N., Margery, J., Guisier, F., Vergnenégre, A., Robinet, G., Auliac, J. B., Gervais, R., & CHOUAID, C. (2017) · Targeted Oncology · doi:10.1007/s11523-017-0510-9 · Cited by 82
Self-citationWang, L., Syn, N. L. X., Subhash, V. V., Any, Y., Thuya, W. L., Cheow, E. S. H., Kong, L. R., Yu, F., Peethala, P. C., Wong, A. L., et al. (2018) · Cancer Letters · doi:10.1016/j.canlet.2017.12.030 · Cited by 82
Shaurova, T., Zhang, L., Goodrich, D. W., & Hershberger, P. A. (2020) · Frontiers in Genetics · doi:10.3389/fgene.2020.00281 · Cited by 82
Bazhenova, L. A., Minchom, A. R., Viteri, S., Bauml, J. M., Ou, S. I., Gadgeel, S. M., Trigo, J. M., Backenroth, D., Li, T. M. W. Y., Londhe, A., et al. (2021) · Lung Cancer · doi:10.1016/j.lungcan.2021.10.020 · Cited by 82
Chen, Y., Hsieh, M., Wu, S., Chang, Y., Shih, J., Liu, Y., Tsai, M., Tsai, T.-H., Yu, C., Yang, J. C., et al. (2014) · Journal of Thoracic Oncology · doi:10.1097/jto.0000000000000232 · Cited by 82
Germline EGFR T790M Mutation Found in Multiple Members of a Familial Cohort
Yu, H. A., Arcila, M. E., Fleischut, M. H., Stadler, Z. K., Ladanyi, M., Berger, M. F., Robson, M. E., & Riely, G. J. (2014) · Journal of Thoracic Oncology · doi:10.1097/jto.0000000000000052 · Cited by 82
Karachaliou, N., CHAIB-OUKADOUR, I., Cardona, A. F., Berenguer, J., Bracht, J. W. P., Yang, J., Cai, X., Wang, Z., Hu, C., Drozdowskyj, A., et al. (2018) · EBioMedicine · doi:10.1016/j.ebiom.2018.02.001 · Cited by 82
Self-citationChen, H., & Cheng, X. (2014) · OncoTargets and Therapy · doi:10.2147/ott.s66502 · Cited by 81
Hu, J. R., Wang, Y., Zhang, Y., Yu, Y., Chen, H., Liu, K., Yao, M., Wang, K., Gu, W., & Shou, T. (2019) · Cancer Medicine · doi:10.1002/cam4.2199 · Cited by 81
Saad, E. D., & Buyse, M. E. (2015) · Annals of Oncology · doi:10.1093/annonc/mdv562 · Cited by 81
Schmid, S., Gautschi, O. P., Rothschild, S. I., Mark, M. T., Froesch, P., Klingbiel, D., Reichegger, H., Jochum, W., Diebold, J., & Früh, M. (2016) · Journal of Thoracic Oncology · doi:10.1016/j.jtho.2016.12.003 · Cited by 81
Activation of RAS family members confers resistance to ROS1 targeting drugs
Cargnelutti, M., Corso, S., Pergolizzi, M., Mévellec, L., Aisner, D. L., Dziadziuszko, R., Varella‐Garcia, M., Comoglio, P. M., Doebele, R. C., Vialard, J. E., et al. (2014) · Oncotarget · doi:10.18632/oncotarget.3311 · Cited by 80
Bertolini, F., Spallanzani, A., Fontana, A., Depenni, R., & Luppi, G. (2015) · CNS Oncology · doi:10.2217/cns.14.51 · Cited by 80
Yu, H. A., Riely, G. J., & Lovly, C. M. (2014) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-13-2437 · Cited by 80
Targeted therapies in development for non-small cell lung cancer
Dy, G. K., & Reungwetwattana, T. (2013) · Journal of Carcinogenesis · doi:10.4103/1477-3163.123972 · Cited by 80
Metadata
- Authors
- Rosell, R., Carcereny, E., Gervais, R., Vergnenegre, A., Massuti, B., Felip, E., Palmero, R., Garcia-Gomez, R., Pallares, C., Sanchez, J. M., Porta, R., Cobo, M., Garrido, P., Longo, F., Moran, T., Insa, A., De Marinis, F., Corre, R., Bover, I., Illiano, A., Dansin, E., de Castro, J., Milella, M., Reguart, N., Altavilla, G., Jimenez, U., Provencio, M., Moreno, M. A., Terrasa, J., Muñoz-Langa, J., Valdivia, J., Isla, D., Domine, M., Molinier, O., Mazieres, J., Baize, N., Garcia-Campelo, R., Robinet, G., Rodriguez-Abreu, D., Lopez-Vivanco, G., Gebbia, V., Ferrera-Delgado, L., Bombaron, P., Bernabe, R., Bearz, A., Artal, A., Cortesi, E., Rolfo, C., Sanchez-Ronco, M., Drozdowskyj, A., Queralt, C., de Aguirre, I., Ramirez, J. L., Sanchez, J. J., Molina, M. A., Taron, M., & Paz-Ares, L.
- Affiliations
- Institut Català d'Oncologia (ES)
- Centre François Baclesse (FR)
- Vall d'Hebron Hospital Universitari (ES)
- Hospital Universitario Ramón y Cajal (ES)
- Policlinico Umberto I (IT)
- Hospital Clínico Universitario de Valencia (ES)
- Hôpital Pontchaillou (FR)
- Hospital Son Llatzer (ES)
- Azienda Ospedaliera Universitaria Policlinico "G. Martino" (IT)
- Hospital Universitario Puerta de Hierro Majadahonda (ES)
- Hospital Universitario Son Dureta (ES)
- Hospital Universitario Virgen de las Nieves (ES)
- Hospital Clínico Universitario Lozano Blesa (ES)
- Centre Hospitalier du Mans (FR)
- Centre Hospitalier Universitaire d'Angers (FR)
- La Maddalena (IT)
- Hospital Universitario Nuestra Señora de Candelaria (ES)
- Centre Hospitalier de Mulhouse (FR)
- Centro di Riferimento Oncologico (IT)
- Hospital Universitario Miguel Servet (ES)
- Sapienza University of Rome (IT)
- Clinica Rotger (ES)
- Pivotal (Spain) (ES)
- Hospital Universitario Virgen del Rocío (ES)
- Corresponding author
- Rosell, Rafael
- ORCID
- Rosell, Rafael
- Carcereny, Enric
- Gervais, Radj
- Felip, Enriqueta
- Cobo, Manuel
- Garrido, Pilar
- Longo, Flavia
- Insa, Amelia
- Corre, Romain
- Altavilla, Giuseppe
- Provencio, Mariano
- Valdivia, Javier
- Isla, Dolores
- Molinier, Olivier
- Gebbia, Vittorio
- Bearz, Alessandra
- Artal, Angel
- Cortesi, Enrico
- Rolfo, Christian
- Queralt, Cristina
- Paz-Ares, Luis
- Venue
- The Lancet Oncology
- Publisher
- Elsevier BV
- Published
- 2012-03
- Volume
- 13
- Issue
- 3
- Pages
- 239-246
- ISSN
- 1470-2045 (ISSN-L)
- OpenAlex
- W2111662961
- Cited by
- 5,489
- References
- 23
- Citations by year
- 2026: 92 · 2025: 169 · 2024: 216 · 2023: 269 · 2022: 367 · 2021: 422 · 2020: 441 · 2019: 440 · 2018: 498 · 2017: 534 · 2016: 509 · 2015: 537 · 2014: 448 · 2013: 401 · 2012: 138
- FWCI
- 392.78
- Type
- journal article
- Language
- en
- Open access
- green
- hdl.handle.net
- Licence
- Locations
- The Lancet Oncology (publishedVersion)
- PubMed (publishedVersion)
- LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (submittedVersion, other-oa)
- IRIS Research product catalog (Sapienza University of Rome) (submittedVersion)
- RUNA. Repositorio Institucional del Sergas (Servicio Gallego de Salud (SERGAS)) (submittedVersion, other-oa)
- 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
- erlotinib, EGFR-mutant non-small cell lung cancer, first-line therapy, exon 19 deletion, L858R mutation, cisplatin, docetaxel, gemcitabine, carboplatin, progression-free survival, targeted therapy, European patients, drug safety, adverse events, treatment discontinuation, EGFR tyrosine kinase inhibitors
- MeSH terms
- Erlotinib Hydrochloride, Docetaxel, Gemcitabine, Administration, Oral, Aged, Antineoplastic Combined Chemotherapy Protocols, Carcinoma, Non-Small-Cell Lung, Cisplatin, Deoxycytidine, Drug Administration Schedule, Europe, Exons, Female, Humans, Lung Neoplasms, Male, Middle Aged, Mutation, Prospective Studies, Quinazolines, Time Factors, Chi-Square Distribution, Proportional Hazards Models, Carboplatin, Treatment Outcome, Disease-Free Survival, Patient Selection, Taxoids, Protein Kinase Inhibitors, Kaplan-Meier Estimate, Precision Medicine, Molecular Targeted Therapy, ErbB Receptors
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
