Cited by 1,083Lung Cancer Treatments and MutationsHER2/EGFR in Cancer ResearchCancer Genomics and Diagnostics

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Rational, biologically based treatment of EGFR-mutant non-small-cell lung cancer

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Pao, William, Chmielecki, Juliann·2010·Nature Reviews Cancer

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Abstract

Epidermal growth factor receptor (EGFR)-mutant non-small-cell lung cancer (NSCLC) was first recognized in 2004 as a distinct, clinically relevant molecular subset of lung cancer. The disease has been the subject of intensive research at both the basic scientific and clinical levels, becoming a paradigm for how to understand and treat oncogene-driven carcinomas. Although patients with EGFR-mutant tumours have increased sensitivity to tyrosine kinase inhibitors (TKIs), primary and acquired resistance to these agents remains a major clinical problem. This Review summarizes recent developments aimed at treating and ultimately curing the disease.

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Pettersen, E. F., Goddard, T. D., Huang, C. C., Couch, G. S., Greenblatt, D. M., Meng, E. C., & Ferrin, T. E. (2004) · Journal of Computational Chemistry · doi:10.1002/jcc.20084 · Cited by 45,882
New response evaluation criteria in solid tumours: revised RECIST guideline (version 1.1)
Eisenhauer, E. A., Therasse, P., Bogaerts, J., Schwartz, L. H., Sargent, D., Ford, R., Dancey, J., Arbuck, S., Gwyther, S., Mooney, M., et al. (2009) · European Journal of Cancer · doi:10.1016/j.ejca.2008.10.026 · Cited by 29,534
Activating Mutations in the Epidermal Growth Factor Receptor Underlying Responsiveness of Non–Small-Cell Lung Cancer to Gefitinib
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
Mutations of the BRAF gene in human cancer
Davies, H., Bignell, G. R., Cox, C., Stephens, P., Edkins, S., Clegg, S., Teague, J., Woffendin, H., Garnett, M. J., Bottomley, W., et al. (2002) · Nature · doi:10.1038/nature00766 · Cited by 10,674 · cited 1×
“Approximately 2–3% of NSCLCs harbour mutations in BRAF , which encodes a signalling molecule downstream of EGF”
Background
Cancer statistics, 2009
Jemal, A., Siegel, R., Ward, E., Hao, Y., Xu, J., & Thun, M. J. (2009) · CA: A Cancer Journal for Clinicians · doi:10.3322/caac.20006 · Cited by 9,709
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
Paclitaxel–Carboplatin Alone or with Bevacizumab for Non–Small-Cell Lung Cancer
Sandler, A., Gray, R., Perry, M. C., Brahmer, J., Schiller, J. H., Dowlati, A., Lilenbaum, R., & Johnson, D. H. (2006) · New England Journal of Medicine · doi:10.1056/nejmoa061884 · Cited by 5,761
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
Identification of the transforming EML4–ALK fusion gene in non-small-cell lung cancer
Soda, M., Choi, Y. L., Enomoto, M., Takada, S., Yamashita, Y., Ishikawa, S., Fujiwara, S.-I., Watanabe, H., Kurashina, K., Hatanaka, H., et al. (2007) · Nature · doi:10.1038/nature05945 · Cited by 5,439 · cited 1×
“Another 5% of tumours harbour translocations in anaplastic lymphoma kinase ( ALK”
Background
Erlotinib in Previously Treated Non–Small-Cell Lung Cancer
Shepherd, F. A., Rodrigues Pereira, J., Ciuleanu, T., Tan, E. H., Hirsh, V., Thongprasert, S., Campos, D., Maoleekoonpiroj, S., Smylie, M., Martins, R., et al. (2005) · New England Journal of Medicine · doi:10.1056/nejmoa050753 · Cited by 5,419
Radiotherapy plus Cetuximab for Squamous-Cell Carcinoma of the Head and Neck
Bonner, J. A., Harari, P. M., Giralt, J., Azarnia, N., Shin, D. M., Cohen, R. B., Jones, C. U., Sur, R. K., Raben, D., Jassem, J., et al. (2006) · New England Journal of Medicine · doi:10.1056/nejmoa053422 · Cited by 5,109 · cited 1×
“The antibody has been US Food and Drug Administration (FDA) approved for the treatment of colorectal and head and neck cancer”
Background
Comparison of Four Chemotherapy Regimens for Advanced Non–Small-Cell Lung Cancer
Schiller, J. H., Harrington, D., Belani, C. P., Langer, C., Sandler, A., Krook, J., Zhu, J., & Johnson, D. H. (2002) · New England Journal of Medicine · doi:10.1056/nejmoa011954 · Cited by 4,955
MET Amplification Leads to Gefitinib Resistance in Lung Cancer by Activating ERBB3 Signaling
Engelman, J. A., Zejnullahu, K., Mitsudomi, T., Song, Y., Hyland, C., Park, J. O., Lindeman, N., Gale, C.-M., Zhao, X., Christensen, J., et al. (2007) · Science · doi:10.1126/science.1141478 · Cited by 4,496
EGF receptor gene mutations are common in lung cancers from “never smokers” and are associated with sensitivity of tumors to gefitinib and erlotinib
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
Self-citation
Gefitinib versus cisplatin plus docetaxel in patients with non-small-cell lung cancer harbouring mutations of the epidermal growth factor receptor (WJTOG3405): an open label, randomised phase 3 trial
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
EGFR Mutation and Resistance of Non–Small-Cell Lung Cancer to Gefitinib
Kobayashi, S., Boggon, T. J., Dayaram, T., Jänne, P. A., Kocher, O., Meyerson, M., Johnson, B. E., Eck, M. J., Tenen, D. G., & Halmos, B. (2005) · New England Journal of Medicine · doi:10.1056/nejmoa044238 · Cited by 3,964
Cetuximab and Chemotherapy as Initial Treatment for Metastatic Colorectal Cancer
Van Cutsem, E., Köhne, C.-H., Hitre, E., Zaluski, J., Chang Chien, C.-R., Makhson, A., D'Haens, G., Pintér, T., Lim, R., Bodoky, G., et al. (2009) · New England Journal of Medicine · doi:10.1056/nejmoa0805019 · Cited by 3,877
COMPARISON OF FOUR CHEMOTHERAPY REGIMENS FOR ADVANCED NON-SMALL-CELL LUNG CANCER
Chiller, J. O. H. S., Arrington, D. A. H., Elani, C. H. P. B., Anger, C., Andler, A. L. S., Rook, J. A. K., Hu, J., & Ohnson, D. A. H. J. (2002) · Cited by 3,730
The IASLC Lung Cancer Staging Project: Proposals for the Revision of the TNM Stage Groupings in the Forthcoming (Seventh) Edition of the TNM Classification of Malignant Tumours
Goldstraw, P., Crowley, J., Chansky, K., Giroux, D. J., Groome, P. A., Rami-Porta, R., Postmus, P. E., Rusch, V., & Sobin, L. (2007) · Journal of Thoracic Oncology · doi:10.1097/jto.0b013e31812f3c1a · Cited by 3,655
Acquired Resistance of Lung Adenocarcinomas to Gefitinib or Erlotinib Is Associated with a Second Mutation in the EGFR Kinase Domain
Pao, W., Miller, V. A., Politi, K. A., Riely, G. J., Somwar, R., Zakowski, M. F., Kris, M. G., & Varmus, H. (2005) · PLoS Medicine · doi:10.1371/journal.pmed.0020073 · Cited by 3,527 · cited 1×
“Unlike CML and GIST, in which the gatekeeper mutation is found in 20–25% of patients with acquired resistance to imatinib, the T790M mutation in EGFR is found in 50% of EGFR -mutant tumours with acquired resistance to erlotinib or gefitini”
BackgroundSelf-citation
ERBB receptors and cancer: the complexity of targeted inhibitors
Hynes, N. E., & Lane, H. A. (2005) · Nature reviews. Cancer · doi:10.1038/nrc1609 · Cited by 3,379
Wild-Type KRAS Is Required for Panitumumab Efficacy in Patients With Metastatic Colorectal Cancer
Amado, R. G., Wolf, M., Peeters, M., Van Cutsem, E., Siena, S., Freeman, D. J., Juan, T., Sikorski, R., Suggs, S., Radinsky, R., et al. (2008) · Journal of Clinical Oncology · doi:10.1200/jco.2007.14.7116 · Cited by 3,207
Epidermal growth factor receptor mutations in lung cancer
Sharma, S. V., Bell, D. W., Settleman, J., & Haber, D. A. (2007) · Nature Reviews Cancer · doi:10.1038/nrc2088 · Cited by 3,170 · cited 1×
“gov/drugdictionary/?CdrID=453548">neratinib ; Wyeth), showed promising preclinical result”
Clinical Resistance to STI-571 Cancer Therapy Caused by BCR-ABL Gene Mutation or Amplification
Gorre, M. E., Mohammed, M., Ellwood, K., Hsu, N., Paquette, R., Rao, P. N., & Sawyers, C. L. (2001) · Science · doi:10.1126/science.1062538 · Cited by 3,104 · cited 1×
“When tumours relapse, a common mechanism of resistance is the emergence of second-site mutations in ABL and KIT”
Background
Multi-Institutional Randomized Phase II Trial of Gefitinib for Previously Treated Patients With Advanced Non–Small-Cell Lung Cancer
Fukuoka, M., Yano, S., Giaccone, G., Tamura, T., Nakagawa, K., Douillard, J., Nishiwaki, Y., Vansteenkiste, J., Kudoh, S., Rischin, D., et al. (2003) · Journal of Clinical Oncology · doi:10.1200/jco.2003.10.038 · Cited by 2,871
A Chromatin-Mediated Reversible Drug-Tolerant State in Cancer Cell Subpopulations
Sharma, S. V., Lee, D. Y., Li, B., Quinlan, M. P., Takahashi, F., Maheswaran, S., McDermott, U., Azizian, N., Zou, L., Fischbach, M. A., et al. (2010) · Cell · doi:10.1016/j.cell.2010.02.027 · Cited by 2,770
Somatic mutations affect key pathways in lung adenocarcinoma
Ding, L., Getz, G., Wheeler, D. A., Mardis, E. R., McLellan, M. D., Cibulskis, K., Sougnez, C., Greulich, H., Muzny, D. M., Morgan, M. B., et al. (2008) · Nature · doi:10.1038/nature07423 · Cited by 2,681 · cited 1×
“Multiple genomic studies have shown that EGFR -mutant NSCLCs represent distinct disease phenotypes that have unique expression, mutation and copy number signature”
BackgroundSelf-citation
Efficacy of Gefitinib, an Inhibitor of the Epidermal Growth Factor Receptor Tyrosine Kinase, in Symptomatic Patients With Non–Small Cell Lung Cancer: A Randomized Trial
Kris, M. G., Natale, R. B., Herbst, R. S., Lynch, Jr., Prager, D., Belani, C. P., Schiller, J. H., Kelly, K., Spiridonidis, H., Sandler, A., et al. (2003) · JAMA · doi:10.1001/jama.290.16.2149 · Cited by 2,517
Clinical and biological features associated with epidermal growth factor receptor gene mutations in lung cancers
Shigematsu, H., Lin, L., Takahashi, T., Nomura, M., Suzuki, M., Wistuba, I. I., Fong, K. M., Lee, H., Toyooka, S., Shimizu, N., et al. (2005) · JNCI Journal of the National Cancer Institute · doi:10.1093/jnci/dji055 · Cited by 2,377
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
Global Survey of Phosphotyrosine Signaling Identifies Oncogenic Kinases in Lung Cancer
Rikova, K., Guo, A., Zeng, Q., Possemato, A., Yu, J., Haack, H., Nardone, J., Lee, K., Reeves, C., Li, Y., et al. (2007) · Cell · doi:10.1016/j.cell.2007.11.025 · Cited by 2,317 · cited 1×
“Another 5% of tumours harbour translocations in anaplastic lymphoma kinase ( ALK”
Background
The T790M mutation in EGFR kinase causes drug resistance by increasing the affinity for ATP
Yun, C.-H., Mengwasser, K. E., Toms, A. V., Woo, M. S., Greulich, H., Wong, K.-K., Meyerson, M., & Eck, M. J. (2008) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0709662105 · Cited by 2,118 · cited 1×
“The crystal structures of the L858R and G719S TKI-sensitive EGFR mutants show that these substitutions activate the kinase through disruption of autoinhibitory interactions, resulting in receptors with 50-fold more activity compared with their wild-type counterpart”
Background
Gefitinib plus best supportive care in previously treated patients with refractory advanced non-small-cell lung cancer: results from a randomised, placebo-controlled, multicentre study (Iressa Survival Evaluation in Lung Cancer)
Thatcher, N., Chang, A., Parikh, P., Rodrigues Pereira, J., Ciuleanu, T., von Pawel, J., Thongprasert, S., Tan, E. H., Pemberton, K., Archer, V., et al. (2005) · The Lancet · doi:10.1016/s0140-6736(05)67625-8 · Cited by 2,079
Cetuximab for the Treatment of Colorectal Cancer
Jonker, D. J., O'Callaghan, C. J., Karapetis, C. S., Zalcberg, J. R., Tu, D., Au, H.-J., Berry, S. R., Krahn, M., Price, T., Simes, R. J., et al. (2007) · New England Journal of Medicine · doi:10.1056/nejmoa071834 · Cited by 1,904
Clinical Features and Outcome of Patients With Non–Small-Cell Lung Cancer Who Harbor EML4-ALK
Shaw, A. T., Yeap, B. Y., Mino-Kenudson, M. A., Digumarthy, S. R., Costa, D. B., Heist, R. S., Solomon, B., Stubbs, H., Admane, S., McDermott, U., et al. (2009) · Journal of Clinical Oncology · doi:10.1200/jco.2009.22.6993 · Cited by 1,873 · cited 1×
“Clinically, ALK fusion-positive tumours are insensitive to EGFR TKI”
Background
RAF inhibitors transactivate RAF dimers and ERK signalling in cells with wild-type BRAF
Poulikakos, P. I., Zhang, C., Bollag, G. E., Shokat, K. M., & Rosen, N. X. (2010) · Nature · doi:10.1038/nature08902 · Cited by 1,841 · cited 1×
“, and confers sensitivity to specific small-molecule V600E inhibitor”
Background
Erlotinib in Lung Cancer — Molecular and Clinical Predictors of Outcome
Tsao, M., Sakurada, A., Cutz, J.-C., Zhu, C., Kamel‐Reid, S., Squire, J. A., Lorimer, I. A. J., Zhang, T., Liu, G., Daneshmand, M., et al. (2005) · New England Journal of Medicine · doi:10.1056/nejmoa050736 · Cited by 1,815
Addiction to Oncogenes--the Achilles Heal of Cancer
Weinstein, I. B. (2002) · Science · doi:10.1126/science.1073096 · Cited by 1,764
Gefitinib in Combination With Gemcitabine and Cisplatin in Advanced Non–Small-Cell Lung Cancer: A Phase III Trial—INTACT 1
Giaccone, G., Herbst, R. S., Manegold, C., Scagliotti, G. V., Rosell, R., Miller, V. A., Natale, R. B., Schiller, J. H., von Pawel, J., Pluzanska, A., et al. (2004) · Journal of Clinical Oncology · doi:10.1200/jco.2004.08.001 · Cited by 1,712
Gefitinib in Combination With Paclitaxel and Carboplatin in Advanced Non–Small-Cell Lung Cancer: A Phase III Trial—INTACT 2
Herbst, R. S., Giaccone, G., Schiller, J. H., Natale, R. B., Miller, V. A., Manegold, C., Scagliotti, G. V., Rosell, R., Oliff, I. A., Reeves, J. A., et al. (2004) · Journal of Clinical Oncology · doi:10.1200/jco.2004.07.215 · Cited by 1,701
Detection of Mutations in EGFR in Circulating Lung-Cancer Cells
Maheswaran, S., Sequist, L. V., Nagrath, S., Ulkus, L., Brannigan, B., Collura, C. V., Inserra, E., Diederichs, S., Iafrate, A. J., Bell, D. W., et al. (2008) · New England Journal of Medicine · doi:10.1056/nejmoa0800668 · Cited by 1,617
Multiple BCR-ABL kinase domain mutations confer polyclonal resistance to the tyrosine kinase inhibitor imatinib (STI571) in chronic phase and blast crisis chronic myeloid leukemia
Shah, N. P., Nicoll, J. M., Nagar, B., Gorre, M. E., PAQUETTE, R. L., Kuriyan, J., & Sawyers, C. L. (2002) · Cancer Cell · doi:10.1016/s1535-6108(02)00096-x · Cited by 1,614
MET amplification occurs with or without T790M mutations in EGFR mutant lung tumors with acquired resistance to gefitinib or erlotinib
Bean, J., Brennan, C., Shih, J.-Y., Riely, G., Viale, A., Wang, L., Chitale, D., Motoi, N., Szoke, J., Broderick, S., et al. (2007) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0710370104 · Cited by 1,598 · cited 1×
“In patients, the major mechanisms of primary and acquired resistance (see below) are the same for both drug”
BackgroundSelf-citation
Epidermal Growth Factor Receptor Gene and Protein and Gefitinib Sensitivity in Non–Small-Cell Lung Cancer
Cappuzzo, F., Hirsch, F. R., Rossi, E., Bartolini, S., Ceresoli, G. L., Bemis, L., Haney, J., Witta, S. E., Danenberg, K. D., Domenichini, I., et al. (2005) · JNCI Journal of the National Cancer Institute · doi:10.1093/jnci/dji112 · Cited by 1,538
Cetuximab in the treatment of colorectal cancer.
Goldberg, R. M., Venook, A. P., & Schilsky, R. L. (2004) · PubMed · Cited by 1,518
KRAS Mutations and Primary Resistance of Lung Adenocarcinomas to Gefitinib or Erlotinib
Pao, W. J., Wang, T. Y., Riely, G. J., Miller, V. A., Pan, Q., Ladanyi, M., Zakowski, M. F., Heelan, R. T., Kris, M. G., & VARMUS, H. E. (2005) · PLoS Medicine · doi:10.1371/journal.pmed.0020017 · Cited by 1,517 · cited 1×
“The initial observation that KRAS -mutant lung tumours are resistant to EGFR TKI”
BackgroundSelf-citation
TRIBUTE: a phase III trial of erlotinib hydrochloride (OSI-774) combined with carboplatin and paclitaxel chemotherapy in advanced non-small-cell lung cancer
Herbst, R. S., Prager, D., Hermann, R., Fehrenbacher, L., Johnson, B. E., Sandler, A., Kris, M. G., Tran, H. T., Klein, P., Li, X., et al. (2005) · Journal of Clinical Oncology · doi:10.1200/jco.2005.02.840 · Cited by 1,490
Mutations in the Epidermal Growth Factor Receptor and in KRAS Are Predictive and Prognostic Indicators in Patients With Non–Small-Cell Lung Cancer Treated With Chemotherapy Alone and in Combination With Erlotinib
Eberhard, D. A., Johnson, B. E., Amler, L. C., Goddard, A. D., Heldens, S., Herbst, R. S., Ince, W. L., Janne, P. A., Januario, T., Johnson, D. H., et al. (2005) · Journal of Clinical Oncology · doi:10.1200/jco.2005.02.857 · Cited by 1,453
BIBW2992, an irreversible EGFR/HER2 inhibitor highly effective in preclinical lung cancer models
Li, D., Ambrogio, L., Shimamura, T., Kubo, S., Takahashi, M., Chirieac, L. R., Padera, R. F., Shapiro, G. I., Baum, A., Himmelsbach, F., et al. (2008) · Oncogene · doi:10.1038/onc.2008.109 · Cited by 1,447 · cited 1×
“gov/drugdictionary/?CdrID=537572">BIBW2992 (afatinib; Boehringer Ingelheim) has potent activity against EGFR and ERBB2 and can overcome T790M-mediated resistance in vitro and in viv o”
Background
Cetuximab plus chemotherapy in patients with advanced non-small-cell lung cancer (FLEX): an open-label randomised phase III trial
Pirker, R., Pereira, J. R., Szczęsna, A., von Pawel, J., Krzakowski, M. J., Ramlau, R., Vynnychenko, I. O., Park, K., Yu, C.-T., Ganul, V., et al. (2009) · The Lancet · doi:10.1016/s0140-6736(09)60569-9 · Cited by 1,346
BRAF mutation predicts sensitivity to MEK inhibition
Solit, D. B., Garraway, L. A., Pratilas, C. A., Sawai, A., Getz, G. A., Basso, A., Ye, Q., Lobo, J. M., She, Y., Osman, I., et al. (2005) · Nature · doi:10.1038/nature04304 · Cited by 1,326
Gefitinib versus docetaxel in previously treated non-small-cell lung cancer (INTEREST): a randomised phase III trial
Kim, E. S., Hirsh, V., Mok, T. S. K., Socinski, M. A., Gervais, R., Wu, Y.-L. L. C., Li, L.-Y., Watkins, C. L., Sellers, M. V., Lowe, E., et al. (2008) · The Lancet · doi:10.1016/s0140-6736(08)61758-4 · Cited by 1,241
Structures of Lung Cancer-Derived EGFR Mutants and Inhibitor Complexes: Mechanism of Activation and Insights into Differential Inhibitor Sensitivity
Yun, C.-H., Boggon, T. J., Li, Y., Woo, M. S., Greulich, H., Meyerson, M., & Eck, M. J. (2007) · Cancer Cell · doi:10.1016/j.ccr.2006.12.017 · Cited by 1,192
New driver mutations in non-small-cell lung cancer
Pao, W. J., & Girard, N. (2011) · The Lancet Oncology · doi:10.1016/s1470-2045(10)70087-5 · Cited by 1,188
Self-citation
Structural basis for inhibition of the epidermal growth factor receptor by cetuximab
Li, S., Schmitz, K. R., Jeffrey, P. D., Wiltzius, J. J. W., Kussie, P. H., & Ferguson, K. M. (2005) · Cancer Cell · doi:10.1016/j.ccr.2005.03.003 · Cited by 1,117 · cited 1×
“As cetuximab interferes with EGFR ligand binding and subsequent receptor dimerization, EGFR mutations that confer ligand independence may abrogate the efficacy of this agen”
Background
Characterizing the cancer genome in lung adenocarcinoma
Weir, B. A., Woo, M. S., Getz, G., Perner, S., Ding, L., Beroukhim, R., Lin, W. M., Province, M. A., Kraja, A., Johnson, L. A., et al. (2007) · Nature · doi:10.1038/nature06358 · Cited by 1,105 · cited 1×
“Multiple genomic studies have shown that EGFR -mutant NSCLCs represent distinct disease phenotypes that have unique expression, mutation and copy number signature”
BackgroundSelf-citation
Preexistence and clonal selection of MET amplification in EGFR mutant NSCLC
Turke, A. B., Zejnullahu, K., Wu, Y.-L., Song, Y., Dias-Santagata, D., Lifshits, E., Toschi, L., Rogers, A., Mok, T., Sequist, L., et al. (2010) · Cancer Cell · doi:10.1016/j.ccr.2009.11.022 · Cited by 1,059
BRAF and RAS mutations in human lung cancer and melanoma.
Brose, M. S., Volpe, P., Feldman, M. D., Kumar, M. S., Rishi, I., Gerrero, R. M., Einhorn, E., Herlyn, M., Minna, J. D., Nicholson, A. G., et al. (2002) · PubMed · Cited by 1,048
Novel mutant-selective EGFR kinase inhibitors against EGFR T790M
Zhou, W., Ercan, D., Chen, L., Yun, C.-H., Li, D., Capelletti, M., Cortot, A. B., Chirieac, L., Iacob, R. E., Padera, R., et al. (2009) · Nature · doi:10.1038/nature08622 · Cited by 1,013 · cited 1×
“Recently, a new compound, WZ4002 (Gatekeeper Pharmaceuticals), was discovered through screening different core chemical scaffolds for their ability to fit in the ATP-binding pocket of EGFR specifically in the presence of T790”
Background
Phase I and Pharmacologic Study of OSI-774, an Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitor, in Patients With Advanced Solid Malignancies
Hidalgo, M., Siu, L. L., Nemunaitis, J., Rizzo, J., Hammond, L. A., Takimoto, C., Eckhardt, S. G., Tolcher, A., Britten, C. D., Denis, L., et al. (2001) · Journal of Clinical Oncology · doi:10.1200/jco.2001.19.13.3267 · Cited by 1,001
Irreversible inhibitors of the EGF receptor may circumvent acquired resistance to gefitinib
Kwak, E. L., Sordella, R., Bell, D. W., Godin-Heymann, N., Okimoto, R. A., Brannigan, B. W., Harris, P. L., Driscoll, D. R., Fidias, P. M., Lynch, T. J., et al. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0502860102 · Cited by 966
ZD1839 (Iressa): an orally active inhibitor of epidermal growth factor signaling with potential for cancer therapy.
Wakeling, A. E., Guy, S. P., Woodburn, J. R., Ashton, S. E., Curry, B. J., Barker, A. J., & Gibson, K. H. (2002) · PubMed · doi:10.7270/q2pc374f · Cited by 925
Phase III Study of Erlotinib in Combination With Cisplatin and Gemcitabine in Advanced Non–Small-Cell Lung Cancer: The Tarceva Lung Cancer Investigation Trial
Gatzemeier, U., Pluzanska, A., Szczęsna, A., Kaukel, E., Roubec, J., Rosa, F. D., Milanowski, J., Karnicka-Mlodkowski, H., Pešek, M., Serwatowski, P., et al. (2007) · Journal of Clinical Oncology · doi:10.1200/jco.2005.05.1474 · Cited by 875
Acquired Resistance to Imatinib in Gastrointestinal Stromal Tumor Occurs Through Secondary Gene Mutation
Antonescu, C. R., Besmer, P., Guo, T., Arkun, K., Hom, G., Koryotowski, B., Leversha, M. A., Jeffrey, P. D., DeSantis, D., Singer, S., et al. (2005) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-04-2245 · Cited by 836
New driver mutations in non-small-cell lung cancer
Tanoue, L. T. (2012) · Yearbook of Pulmonary Disease · doi:10.1016/j.ypdi.2012.01.036 · Cited by 833
Drug development of MET inhibitors: targeting oncogene addiction and expedience
Comoglio, P. M., Giordano, S., & Trusolino, L. (2008) · Nature Reviews Drug Discovery · doi:10.1038/nrd2530 · Cited by 832
Novel D761Y and Common Secondary T790M Mutations in Epidermal Growth Factor Receptor–Mutant Lung Adenocarcinomas with Acquired Resistance to Kinase Inhibitors
Balak, M. N., Gong, Y., Riely, G. J., Somwar, R., Li, A. R., Zakowski, M. F., Chiang, A. C., Yang, G., Ouerfelli, O., Kris, M. G., et al. (2006) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-06-1570 · Cited by 823 · cited 1×
“EGFR mutations are usually heterozygous, with the mutant allele also showing gene amplificatio”
BackgroundSelf-citation
Clinical definition of acquired resistance to epidermal growth factor receptor tyrosine kinase inhibitors in non-small-cell lung cancer.
Jackman, D., Pao, W., Riely, G. J., Engelman, J. A., Kris, M. G., Jänne, P. A., Lynch, T., Johnson, B. E., & Miller, V. A. (2010) · Journal of Clinical Oncology · doi:10.1200/jco.2009.24.7049 · Cited by 793 · cited 1×
“To minimize reporting of false-positive and false-negative activity in clinical trials and to facilitate the identification of agents that truly overcome acquired resistance to gefitinib and erlotinib, the following clinical and molecular criteria were recently proposed to more precisely define acquired resistance to…”
BackgroundSelf-citation
Detection of BCR-ABL mutations in patients with CML treated with imatinib is virtually always accompanied by clinical resistance, and mutations in the ATP phosphate-binding loop (P-loop) are associated with a poor prognosis
Branford, S., Rudzki, Z., Walsh, S., Parkinson, I., Grigg, A., Szer, J., Taylor, K. M., Herrmann, R., Seymour, J. F., Arthur, C., et al. (2003) · Blood · doi:10.1182/blood-2002-09-2896 · Cited by 767
ZD1839, a Selective Oral Epidermal Growth Factor Receptor–Tyrosine Kinase Inhibitor, Is Well Tolerated and Active in Patients With Solid, Malignant Tumors: Results of a Phase I Trial
Ranson, M., Hammond, L. A., Ferry, D. K., Kris, M. G., Tullo, A. B., Murray, P. I., Miller, V. A., Averbuch, S. D., Ochs, J., Morris, C. Q., et al. (2002) · Journal of Clinical Oncology · doi:10.1200/jco.2002.10.112 · Cited by 764
Predictive and Prognostic Impact of Epidermal Growth Factor Receptor Mutation in Non–Small-Cell Lung Cancer Patients Treated With Gefitinib
Han, S., Kim, T., Hwang, P. G., Jeong, S., Kim, J., Choi, I. S., Oh, D., Kim, J. H., Kim, D., Chung, D. H., et al. (2005) · Journal of Clinical Oncology · doi:10.1200/jco.2005.01.388 · Cited by 757 · cited 1×
“A small proportion (1–20%, depending on the trial) of patients with no detectable EGFR -activating mutations show a radiographic response when treated with EGFR TKI”
Background
Assessment of somatic k-RAS mutations as a mechanism associated with resistance to EGFR-targeted agents: a systematic review and meta-analysis of studies in advanced non-small-cell lung cancer and metastatic colorectal cancer
Linardou, H., Dahabreh, I. J., Kanaloupiti, D., Siannis, F., Bafaloukos, D., Kosmidis, P., Papadimitriou, C. A., & Murray, S. (2008) · The Lancet Oncology · doi:10.1016/s1470-2045(08)70206-7 · Cited by 739
PF00299804, an Irreversible Pan-ERBB Inhibitor, Is Effective in Lung Cancer Models with EGFR and ERBB2 Mutations that Are Resistant to Gefitinib
Engelman, J. A., Zejnullahu, K., Gale, C.-M., Lifshits, E., Gonzales, A. J., Shimamura, T., Zhao, F., Vincent, P. W., Naumov, G. N., Bradner, J. E., et al. (2007) · Cancer Research · doi:10.1158/0008-5472.can-07-1885 · Cited by 730 · cited 1×
“It has also shown efficacy against H1975 (EGFR L858R and T790M) cells and xenograft model”
Background
Bronchioloalveolar Pathologic Subtype and Smoking History Predict Sensitivity to Gefitinib in Advanced Non–Small-Cell Lung Cancer
Miller, V. A., Kris, M. G., Shah, N., Patel, J. D., Azzoli, C. G., Gomez, J. E., Krug, L. M., Pao, W. J., Rizvi, N. A., Pizzo, B., et al. (2004) · Journal of Clinical Oncology · doi:10.1200/jco.2004.08.158 · Cited by 728 · cited 1×
“( Table 1 ), the major clinical characteristics of responding patients were found to be adenocarcinoma histology, East Asian ethnicity, a history of never smoking cigarettes and female gende”
BackgroundSelf-citation
Epidermal Growth Factor Receptor Targeting in Cancer
Mendelsohn, J. M., & Baselga, J. M. (2006) · Seminars in Oncology · doi:10.1053/j.seminoncol.2006.04.003 · Cited by 705 · cited 1×
“Cetuximab is a human–murine chimeric IgG1 monoclonal antibody that binds to the extracellular domain of EGFR and blocks EGFR signallin”
Background
Molecular predictors of outcome with gefitinib in a phase III placebo-controlled study in advanced non-small-cell lung cancer
Hirsch, F. R., Varella-Garcia, M., Bunn, P. A., Franklin, W. A., Dziadziuszko, R., Thatcher, N., Chang, A., Parikh, P., Pereira, J. R., Ciuleanu, T., et al. (2006) · Journal of Clinical Oncology · doi:10.1200/jco.2006.06.3958 · Cited by 703
Oncogenic Transformation by Inhibitor-Sensitive and -Resistant EGFR Mutants
Greulich, H., Chen, T.-H., Feng, W., Jänne, P. A., Alvarez, J. V., Zappaterra, M., Bulmer, S. E., Frank, D. A., Hahn, W. C., Sellers, W. R., et al. (2005) · PLoS Medicine · doi:10.1371/journal.pmed.0020313 · Cited by 677 · cited 1×
“In vitro studies have shown that such mutations are less sensitive to EGFR TKIs than the exon 19 deletion and L858R mutant”
Background
Anti-tumor activity of GW572016: a dual tyrosine kinase inhibitor blocks EGF activation of EGFR/erbB2 and downstream Erk1/2 and AKT pathways
Xia, W., Mullin, R. J., Keith, B. R., Liu, L.-H., Ma, H., Rusnak, D. W., Owens, G., Alligood, K. J., & Spector, N. L. (2002) · Oncogene · doi:10.1038/sj.onc.1205794 · Cited by 671
Role of KRAS and EGFR As Biomarkers of Response to Erlotinib in National Cancer Institute of Canada Clinical Trials Group Study BR.21
Zhu, C.-Q., da Cunha Santos, G., Ding, K., Sakurada, A., Cutz, J.-C., Liu, N., Zhang, T., Marrano, P., Whitehead, M., Squire, J. A., et al. (2008) · Journal of Clinical Oncology · doi:10.1200/jco.2007.14.8924 · Cited by 661
Structural Basis for the Autoinhibition and STI-571 Inhibition of c-Kit Tyrosine Kinase
Mol, C. D., Dougan, D. R., Schneider, T. R., Skene, R. J., Kraus, M. L., Scheibe, D. N., Snell, G., Zou, H., Sang, B., & Wilson, K. P. (2004) · Journal of Biological Chemistry · doi:10.1074/jbc.m403319200 · Cited by 651
Antitumor Activity of HKI-272, an Orally Active, Irreversible Inhibitor of the HER-2 Tyrosine Kinase
Rabindran, S. K., Discafani, C. M., Rosfjord, E. C., Baxter, M., Floyd, M. B., Golas, J., Hallett, W. A., Johnson, B. D., Nilakantan, R., Overbeek, E., et al. (2004) · Cancer Research · doi:10.1158/0008-5472.can-03-2868 · Cited by 647
Hepatocyte growth factor induces gefitinib resistance of lung adenocarcinoma with epidermal growth factor receptor-activating mutations
Yano, S., Wang, W., Li, Q., Matsumoto, K., Sakurama, H., Nakamura, T., Ogino, H., Kakiuchi, S., Hanibuchi, M., Nishioka, Y., et al. (2008) · Cancer Research · doi:10.1158/0008-5472.can-08-1643 · Cited by 643
Epidermal Growth Factor Receptor Mutations and Gene Amplification in Non–Small-Cell Lung Cancer: Molecular Analysis of the IDEAL/INTACT Gefitinib Trials
Bell, D. W., Lynch, T. J., Haserlat, S. M., Harris, P. L., Okimoto, R. A., Brannigan, B. W., Sgroi, D. C., Muir, B., Riemenschneider, M. J., Iacona, R. B., et al. (2005) · Journal of Clinical Oncology · doi:10.1200/jco.2005.02.7078 · Cited by 598
Increased Epidermal Growth Factor Receptor Gene Copy Number Detected by Fluorescence In Situ Hybridization Associates With Increased Sensitivity to Gefitinib in Patients With Bronchioloalveolar Carcinoma Subtypes: A Southwest Oncology Group Study
Hirsch, F. R., Varella‐Garcia, M., McCoy, J., West, H., Xavier, A. C., Gumerlock, P. H., Bunn, P. A., Franklin, W. A., Crowley, J. J., & Gandara, D. R. (2005) · Journal of Clinical Oncology · doi:10.1200/jco.2005.01.2823 · Cited by 574
Selective Oral Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitor ZD1839 Is Generally Well-Tolerated and Has Activity in Non–Small-Cell Lung Cancer and Other Solid Tumors: Results of a Phase I Trial
Herbst, R. S., Maddox, A., Rothenberg, M. L., Small, E. J., Rubin, E. H., Baselga, J. M., Rojo, F., Hong, W. K., Swaisland, H., Averbuch, S. D., et al. (2002) · Journal of Clinical Oncology · doi:10.1200/jco.2002.03.038 · Cited by 572
Inhibition of drug-resistant mutants of ABL, KIT, and EGF receptor kinases
Carter, T. A., Wodicka, L. M., Shah, N. P., Velasco, A. M., Fabian, M. A., Treiber, D. K., Milanov, Z. V., Atteridge, C. E., Biggs, W., Edeen, P. T., et al. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0504952102 · Cited by 555 · cited 1×
“Second-generation EGFR inhibitors were touted to overcome T790M-mediated resistanc”
BackgroundSelf-citation
Inherited susceptibility to lung cancer may be associated with the T790M drug resistance mutation in EGFR
Bell, D. W., Gore, I., Okimoto, R. A., Godin-Heymann, N., Sordella, R., Mulloy, R., Sharma, S. V., Brannigan, B. W., Mohapatra, G., Settleman, J., et al. (2005) · Nature Genetics · doi:10.1038/ng1671 · Cited by 529 · cited 1×
“This variant seems to be associated with increased genetic susceptibility to lung cancer, which usually occurs after the age of 50 (Ref”
Background
Acquired resistance to EGFR tyrosine kinase inhibitors in cancer cells is mediated by loss of IGF-binding proteins
Guix, M., Faber, A. C., Wang, S. E., Olivares, M. G., Song, Y., Qu, S., Rinehart, C., Seidel, B., Yee, D., Arteaga, C. L., et al. (2008) · Journal of Clinical Investigation · doi:10.1172/jci34588 · Cited by 525 · cited 1×
“Increased IGF1R signalling has also been associated with acquired resistance, albeit only in an in vitro model using a cell line that expressed high levels of wild-type EGF”
Background
Pharmacodynamic Studies of the Epidermal Growth Factor Receptor Inhibitor ZD1839 in Skin From Cancer Patients: Histopathologic and Molecular Consequences of Receptor Inhibition
Albanell, J., Rojo, F., Averbuch, S., Feyereislova, A., Mascaro, J. M., Herbst, R. S., LoRusso, P. M., Rischin, D., Sauleda, S., Gee, J., et al. (2002) · Journal of Clinical Oncology · doi:10.1200/jco.20.1.110 · Cited by 523
BIM Mediates EGFR Tyrosine Kinase Inhibitor-Induced Apoptosis in Lung Cancers with Oncogenic EGFR Mutations
Costa, D. B., Halmos, B., Kumar, A., Schumer, S., Huberman, M. S., Boggon, T. J., Tenen, D. G., & Kobayashi, S. S. (2007) · PLoS Medicine · doi:10.1371/journal.pmed.0040315 · Cited by 511 · cited 1×
“L747 occurs at the start of the loop between the β3 strand and the α-C helix and is thought to shift theequilibrium towards the active conformation of the recepto”
Background
PTEN Loss Contributes to Erlotinib Resistance in EGFR-Mutant Lung Cancer by Activation of Akt and EGFR
Sos, M. L., Koker, M., Weir, B. A., Heynck, S., Rabinovsky, R., Zander, T., Seeger, J. M., Weiss, J., Fischer, F., Frommolt, P., et al. (2009) · Cancer Research · doi:10.1158/0008-5472.can-08-4055 · Cited by 504 · cited 1×
“Similarly, loss of PTEN expression in EGFR -mutant cells correlates with decreased sensitivity to EGFR TKI”
Background
Lung adenocarcinomas induced in mice by mutant EGF receptors foundin human lung cancers respondto a tyrosine kinase inhibitor orto down-regulation of the receptors
Politi, K., Zakowski, M. F., Fan, P.-D., Schonfeld, E. A., Pao, W., & Varmus, H. E. (2006) · Genes & Development · doi:10.1101/gad.1417406 · Cited by 478
Self-citation
The impact of human EGFR kinase domain mutations on lung tumorigenesis and in vivo sensitivity to EGFR-targeted therapies
Ji, H., Li, D., Chen, L., Shimamura, T., Kobayashi, S., McNamara, K., Mahmood, U., Mitchell, A., Sun, Y., Al-Hashem, R., et al. (2006) · Cancer Cell · doi:10.1016/j.ccr.2006.04.022 · Cited by 462 · cited 1×
“Interestingly, in mouse models of lung cancer driven by EGFR-L858R (exon 21), cetuximab can induce dramatic tumour regression”
Background
Allelic dilution obscures detection of a biologically significant resistance mutation in EGFR-amplified lung cancer
Engelman, J. A., Mukohara, T., Zejnullahu, K., Lifshits, E., Borras, A. M., Gale, C.-M., Naumov, G. N., Yeap, B. Y., Jarrell, E., Sun, J., et al. (2006) · Journal of Clinical Investigation · doi:10.1172/jci28656 · Cited by 457 · cited 1×
“The addition of a constitutively active PI3K mutant (E545K) has been shown to confer gefitinib resistance, at least in vitro”
Background
Presence ofEpidermal Growth Factor ReceptorGene T790M Mutation as a Minor Clone in Non–Small Cell Lung Cancer
Inukai, M., Toyooka, S., Ito, S., Asano, H., Ichihara, S., Soh, J., Suehisa, H., Ouchida, M., Aoe, K., Aoe, M., et al. (2006) · Cancer Research · doi:10.1158/0008-5472.can-06-1951 · Cited by 450
Cetuximab and First-Line Taxane/Carboplatin Chemotherapy in Advanced Non–Small-Cell Lung Cancer: Results of the Randomized Multicenter Phase III Trial BMS099
Lynch, T. J., Patel, T., Dreisbach, L., McCleod, M., Heim, W. J., Hermann, R. C., Paschold, E., Iannotti, N. O., Dakhil, S., Gorton, S., et al. (2010) · Journal of Clinical Oncology · doi:10.1200/jco.2009.21.9618 · Cited by 447
Kinetic Analysis of Epidermal Growth Factor Receptor Somatic Mutant Proteins Shows Increased Sensitivity to the Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitor, Erlotinib
Carey, K. D., Garton, A. J., Romero, M. S., Kahler, J., Thomson, S., Ross, S., Park, F., Haley, J. D., Gibson, N., & Sliwkowski, M. X. (2006) · Cancer Research · doi:10.1158/0008-5472.can-06-0453 · Cited by 445 · cited 1×
“The crystal structures of the L858R and G719S TKI-sensitive EGFR mutants show that these substitutions activate the kinase through disruption of autoinhibitory interactions, resulting in receptors with 50-fold more activity compared with their wild-type counterpart”
Background
Neratinib, an Irreversible Pan-ErbB Receptor Tyrosine Kinase Inhibitor: Results of a Phase II Trial in Patients With Advanced Non–Small-Cell Lung Cancer
Sequist, L. V. D., Besse, B., Lynch, T. J., Miller, V. A., Wong, K., Gitlitz, B. J., Eaton, K. D., Zacharchuk, C., Freyman, A., Powell, C., et al. (2010) · Journal of Clinical Oncology · doi:10.1200/jco.2009.27.9414 · Cited by 437
Acquired Resistance to Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitors in Non–Small-Cell Lung Cancers Dependent on the Epidermal Growth Factor Receptor Pathway
Nguyen, K.-S. H., Kobayashi, S., & Costa, D. B. (2009) · Clinical Lung Cancer · doi:10.3816/clc.2009.n.039 · Cited by 437 · cited 1×
“In the past 5 years, however, at least nine prospective single-arm studies for patients with advanced NSCLC and activating EGFR mutations have validated the benefit of EGFR TKIs in EGFR -mutant lung cancer (reviewed in Ref”
Background
Distinct Epidermal Growth Factor Receptor and KRAS Mutation Patterns in Non–Small Cell Lung Cancer Patients with Different Tobacco Exposure and Clinicopathologic Features
Tam, I. Y. S., Chung, L.-P., Suen, W., Wang, E., Wong, M. C. M., Ho, K. K., Lam, W. K., Chiu, S. W., Girard, L., Minna, J. D., et al. (2006) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-05-1981 · Cited by 400
Dual targeting of EGFR can overcome a major drug resistance mutation in mouse models of EGFR mutant lung cancer
Regales, L., Gong, Y., Shen, R., de Stanchina, E., Vivanco, I., Goel, A. J., Koutcher, J. A., Spassova, M. K., Ouerfelli, O., Mellinghoff, I. K., et al. (2009) · Journal of Clinical Investigation · doi:10.1172/jci38746 · Cited by 376 · cited 1×
“Interestingly, in mouse models of lung cancer driven by EGFR-L858R (exon 21), cetuximab can induce dramatic tumour regression”
BackgroundSelf-citation
Polyclonal Evolution of Multiple Secondary KIT Mutations in Gastrointestinal Stromal Tumors under Treatment with Imatinib Mesylate
Wardelmann, E., Merkelbach‐Bruse, S., Pauls, K., Thomas, N., Schildhaus, H., Heinicke, T., Speidel, N., Pietsch, T., Buettner, R., Pink, D., et al. (2006) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-05-1211 · Cited by 363
Gefitinib-Induced Killing of NSCLC Cell Lines Expressing Mutant EGFR Requires BIM and Can Be Enhanced by BH3 Mimetics
Cragg, M. S., Kuroda, J., Puthalakath, H., Huang, D. C. S., & Strasser, A. (2007) · PLoS Medicine · doi:10.1371/journal.pmed.0040316 · Cited by 346
Induction of BIM Is Essential for Apoptosis Triggered by EGFR Kinase Inhibitors in Mutant EGFR-Dependent Lung Adenocarcinomas
Gong, Y., Somwar, R., Politi, K. A., Balak, M. N., Chmielecki, J., Jiang, X., & Pao, W. J. (2007) · PLoS Medicine · doi:10.1371/journal.pmed.0040294 · Cited by 330
Self-citation
A new mutation in the KIT ATP pocket causes acquired resistance to imatinib in a gastrointestinal stromal tumor patient
Tamborini, E., Bonadiman, L., Greco, A., Albertini, V., Negri, T., Gronchi, A., Bertulli, R., Colecchia, M., Casali, P. G., Pierotti, M. A., et al. (2004) · Gastroenterology · doi:10.1053/j.gastro.2004.02.021 · Cited by 323 · cited 1×
“When tumours relapse, a common mechanism of resistance is the emergence of second-site mutations in ABL and KIT”
Background
The Juxtamembrane Region of the EGF Receptor Functions as an Activation Domain
Brewer, M. R., Choi, S. H., Alvarado, D., Moravcevic, K., Pozzi, A., Lemmon, M. A., & Carpenter, G. F. (2009) · Molecular Cell · doi:10.1016/j.molcel.2009.04.034 · Cited by 323
Molecular classification of mucoepidermoid carcinomas—Prognostic significance of the MECT1 – MAML2 fusion oncogene
Behboudi, A., Enlund, F., Winnes, M., Andrén, Y., Nordkvist, A., Leivo, I. V. V., Flaberg, E., Székely, L., Mäkitie, A. A., Grenman, R. A., et al. (2006) · Genes Chromosomes and Cancer · doi:10.1002/gcc.20306 · Cited by 321 · cited 1×
“As MECs harbour a recurrent mucoepidermoid carcinoma translocated 1 ( MECT1 )–mastermind-like 2( MAML2 )fusio”
Background
Lung Cancer with Epidermal Growth Factor Receptor Exon 20 Mutations Is Associated with Poor Gefitinib Treatment Response
Wu, J.-Y., Wu, S.-G., Yang, C.-H., Gow, C.-H., Chang, Y.-L., Yu, C.-J., Shih, J.-Y., & Yang, P.-C. (2008) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-07-5123 · Cited by 319 · cited 1×
“For example, small insertions or duplications in exon 20 (such as D770_N771, ins NPG, ins SVQ, insG and N771T; see Ref”
Background
EML4-ALK: Honing In on a New Target in Non–Small-Cell Lung Cancer
Horn, L., & Pao, W. J. (2009) · Journal of Clinical Oncology · doi:10.1200/jco.2009.23.6661 · Cited by 317 · cited 1×
“Multiple different EML4–ALK variants have been identified, but all involve the tyrosine kinase portion of ALK and have variable lengths of EML4 (Ref”
BackgroundSelf-citation
Differential Effects of Gefitinib and Cetuximab on Non–small-cell Lung Cancers Bearing Epidermal Growth Factor Receptor Mutations
Mukohara, T., Engelman, J. A., Hanna, N. H., Yeap, B. Y., Kobayashi, S. S., Lindeman, N. I., Halmos, B., Pearlberg, J., Tsuchihashi, Z., Cantley, L. C., et al. (2005) · JNCI Journal of the National Cancer Institute · doi:10.1093/jnci/dji238 · Cited by 314
Structure and Clinical Relevance of the Epidermal Growth Factor Receptor in Human Cancer
Kumar, A., Petri, E. T., Halmos, B., & Boggon, T. J. (2008) · Journal of Clinical Oncology · doi:10.1200/jco.2007.12.1178 · Cited by 308 · cited 1×
“D761 occurs in the α-C helix and a salt bridge formed by D761 may be disrupted by mutation to tyrosine, affecting the catalytic cleft of the recepto”
Background
Structural biology contributions to the discovery of drugs to treat chronic myelogenous leukaemia
Cowan‐Jacob, S. W., Fendrich, G., Floersheimer, A., Furet, P., Liebetanz, J., Rummel, G., Rheinberger, P., Centeleghe, M., Fabbro, D., & Manley, P. W. (2006) · Acta Crystallographica Section D Biological Crystallography · doi:10.1107/s0907444906047287 · Cited by 304
A Phase I Study with Neratinib (HKI-272), an Irreversible Pan ErbB Receptor Tyrosine Kinase Inhibitor, in Patients with Solid Tumors
Wong, K.-K., Fracasso, P. M., Bukowski, R. M., Lynch, T. J., Münster, P. N., Shapiro, G. I., Janne, P. A., Eder, J. P., Naughton, M. J., Ellis, M. J., et al. (2009) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-08-1978 · Cited by 301 · cited 1×
“but no responses were reported in a Phase I trial involving 14 patients with NSCLC with EGFR-positive tumours (measured by IHC) and six patients who had previously progressed on erlotinib achieved stable diseas”
Background
Molecular Characteristics of Bronchioloalveolar Carcinoma and Adenocarcinoma, Bronchioloalveolar Carcinoma Subtype, Predict Response to Erlotinib
Miller, V. A., Riely, G. J., Zakowski, M. F., Li, A. R., Patel, J. D., Heelan, R. T., Kris, M. G., Sandler, A. B., Carbone, D. P., Tsao, A. S., et al. (2008) · Journal of Clinical Oncology · doi:10.1200/jco.2007.13.0062 · Cited by 298 · cited 1×
“Erlotinib has similarly been shown to be highly effective in patients with EGFR -mutant tumour”
BackgroundSelf-citation
Prospective Assessment of Discontinuation and Reinitiation of Erlotinib or Gefitinib in Patients with Acquired Resistance to Erlotinib or Gefitinib Followed by the Addition of Everolimus
Riely, G. J., Kris, M. G., Zhao, B., Akhurst, T. J., Milton, D. T., Moore, E., Tyson, L. B., Pao, W. J., Rizvi, N. A., Schwartz, L. H., et al. (2007) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-07-0560 · Cited by 290 · cited 1×
“Following the discontinuation of TKI therapy, disease flares have also been reporte”
BackgroundSelf-citation
Acquired Resistance to Epidermal Growth Factor Receptor Kinase Inhibitors Associated with a Novel T854A Mutation in a Patient with EGFR-Mutant Lung Adenocarcinoma
Bean, J. M., Riely, G. J., Balak, M. N., Marks, J. L., Ladanyi, M., Miller, V. A., & Pao, W. J. (2008) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-08-0151 · Cited by 283
Self-citation
PIK3CA mutation status in Japanese lung cancer patients
Kawano, O., Sasaki, H., Endo, K., Suzuki, E., Haneda, H., Yukiue, H., Kobayashi, Y., Yano, M., & Fujii, Y. (2006) · Lung Cancer · doi:10.1016/j.lungcan.2006.07.006 · Cited by 280 · cited 1×
“For example, mutations in PIK3CA , the p110α catalytic subunit of PI3K, are found in approximately 2% of NSCLCs and can co-occur with EGFR mutation”
Background
Missense mutations of the BRAF gene in human lung adenocarcinoma.
Naoki, K., Chen, T. H., Richards, W. G., Sugarbaker, D. J., & Meyerson, M. M. (2002) · PubMed · Cited by 279
Phase I pharmacokinetic trial of the selective oral epidermal growth factor receptor tyrosine kinase inhibitor gefitinib (‘Iressa’, ZD1839) in Japanese patients with solid malignant tumors
Nakagawa, K., Tamura, T., Negoro, S., Kudoh, S., Yamamoto, N., Yamamoto, N., Takeda, K., Swaisland, H., Nakatani, I., Hirose, M., et al. (2003) · Annals of Oncology · doi:10.1093/annonc/mdg250 · Cited by 277
Epithelial to mesenchymal transition predicts gefitinib resistance in cell lines of head and neck squamous cell carcinoma and non–small cell lung carcinoma
Frederick, B. A., Helfrich, B. A., Coldren, C. D., Zheng, D., Chan, D., Bunn, P. A., & Raben, D. (2007) · Molecular Cancer Therapeutics · doi:10.1158/1535-7163.mct-07-0138 · Cited by 270 · cited 1×
“The epithelial to mesenchymal transition (EMT) has been associated with resistance to EGFR TKIs in vitro”
Background
Combination of EGFR gene copy number and protein expression predicts outcome for advanced non-small-cell lung cancer patients treated with gefitinib
Hirsch, F. R., Varella‐Garcia, M., Cappuzzo, F., McCoy, J., Bemis, L., Xavier, A. C., Dziadziuszko, R., Gumerlock, P. H., Chansky, K., West, H., et al. (2007) · Annals of Oncology · doi:10.1093/annonc/mdm003 · Cited by 270
Prognostic and Therapeutic Implications of EGFR and KRAS Mutations in Resected Lung Adenocarcinoma
Marks, J. L., Broderick, S., Zhou, Q. C., Chitale, D. A., Li, A. R., Zakowski, M. F., Kris, M. G., Rusch, V. W., Azzoli, C. G., Seshan, V., et al. (2008) · Journal of Thoracic Oncology · doi:10.1097/jto.0b013e318160c607 · Cited by 268 · cited 1×
“EGFR -mutant tumours most often display adenocarcinoma histology and are associated with a better prognosis than EGFR wild-type tumour”
BackgroundSelf-citation
Analysis of Potential Predictive Markers of Cetuximab Benefit in BMS099, a Phase III Study of Cetuximab and First-Line Taxane/Carboplatin in Advanced Non–Small-Cell Lung Cancer
Khambata‐Ford, S., Harbison, C. T., Hart, L. L., Awad, M., Xu, L., Horak, C. E., Dakhil, S. R., Hermann, R. C., Lynch, T. J., & Weber, M. R. (2010) · Journal of Clinical Oncology · doi:10.1200/jco.2009.25.2890 · Cited by 265 · cited 1×
“No links between EGFR mutations and sensitivity to cetuximab have been found, although only a limited number of patients has been studie”
Background
Response and resistance in a non-small-cell lung cancer patient with an epidermal growth factor receptor mutation and leptomeningeal metastases treated with high-dose gefitinib
Jackman, D. M., Holmes, A. J., Lindeman, N., Wen, P. Y., Kesari, S., Borras, A. M., Bailey, C., de Jong, F., Jänne, P. A., & Johnson, B. E. (2006) · Journal of Clinical Oncology · doi:10.1200/jco.2006.06.6126 · Cited by 260 · cited 1×
“This observation may be due to a lack of selective pressure, as the concentration of EGFR TKI that reaches the brain is 100-fold less than that found in bloo”
Background
Randomized phase II study of cetuximab plus cisplatin/vinorelbine compared with cisplatin/vinorelbine alone as first-line therapy in EGFR-expressing advanced non-small-cell lung cancer
Rosell, R., Robinet, G., Szczęsna, A., Ramlau, R., Constenla, M., Mennecier, B., Pfeifer, W., O'Byrne, K. J., Welte, T., Kolb, R., et al. (2007) · Annals of Oncology · doi:10.1093/annonc/mdm474 · Cited by 258 · cited 1×
“and, despite cetuximab showing a promising additive effect with chemotherap”
Background
EGFR Mutations in Small-Cell Lung Cancers in Patients Who Have Never Smoked
Zakowski, M. F., Ladanyi, M., & Kris, M. G. (2006) · New England Journal of Medicine · doi:10.1056/nejmc053610 · Cited by 254
Prognostic Implication of EGFR, KRAS, and TP53 Gene Mutations in a Large Cohort of Japanese Patients with Surgically Treated Lung Adenocarcinoma
Kosaka, T., Yatabe, Y., Onozato, R., Kuwano, H., & Mitsudomi, T. (2009) · Journal of Thoracic Oncology · doi:10.1097/jto.0b013e3181914111 · Cited by 253 · cited 1×
“Clinically, the prognostic value of the EGFR mutation in patients undergoing surgery is approximately the same in Japan and the United State”
Background
Genetic Predictors of MEK Dependence in Non–Small Cell Lung Cancer
Pratilas, C. A., Hanrahan, A. J., Halilovic, E., Persaud, Y., Soh, J., Chitale, D. A., Shigematsu, H., Yamamoto, H., Sawai, A., Janakiraman, M., et al. (2008) · Cancer Research · doi:10.1158/0008-5472.can-08-2223 · Cited by 252 · cited 1×
“gov/drugdictionary/?CdrID=456780">PD0325901 but are resistant to EGFR inhibitio”
BackgroundSelf-citation
Potent, transient inhibition of BCR-ABL with dasatinib 100 mg daily achieves rapid and durable cytogenetic responses and high transformation-free survival rates in chronic phase chronic myeloid leukemia patients with resistance, suboptimal response or intolerance to imatinib
Shah, N. P., Kim, D.-W., Kantarjian, H. M., Rousselot, P. H., Llacer, P. E. D., Enrico, A. I., Vela‐Ojeda, J., Silver, R. T., Khoury, H. J., Muller, M. C., et al. (2010) · Haematologica · doi:10.3324/haematol.2009.011452 · Cited by 245 · cited 1×
“gov/drugdictionary/?CdrID=315885">dasatinib (Sprycel; Bristol–Myers Squibb) induced similar killing rates as chronic exposur”
Background
Bronchial and Peripheral Murine Lung Carcinomas Induced by T790M-L858R Mutant EGFR Respond to HKI-272 and Rapamycin Combination Therapy
Li, D., Shimamura, T., Ji, H., Chen, L., Haringsma, H. J., McNamara, K. L., Liang, M., Perera, S. A., Zaghlul, S., Borgman, C. L., et al. (2007) · Cancer Cell · doi:10.1016/j.ccr.2007.06.005 · Cited by 243 · cited 1×
“gov/drugdictionary/?CdrID=42555">rapamycin resulted in greater tumour shrinkage than either agent alone in transgenic mice with T790M-containing lung tumour”
Background
Specific EGFR Mutations Predict Treatment Outcome of Stage IIIB/IV Patients With Chemotherapy-Naive Non–Small-Cell Lung Cancer Receiving First-Line Gefitinib Monotherapy
Yang, C.-H., Yu, C., Shih, J., Chang, Y., Hu, F., Tsai, M.-C., Chen, K., Lin, Z., Huang, C.-J., Shun, C., et al. (2008) · Journal of Clinical Oncology · doi:10.1200/jco.2007.15.6695 · Cited by 238 · cited 1×
“A small proportion (1–20%, depending on the trial) of patients with no detectable EGFR -activating mutations show a radiographic response when treated with EGFR TKI”
BackgroundSelf-citation
A Phase II Study of PD-0325901, an Oral MEK Inhibitor, in Previously Treated Patients with Advanced Non–Small Cell Lung Cancer
Haura, E. B., Ricart, A. D., Larson, T. G., Stella, P. J., Bazhenova, L., Miller, V. A., Cohen, R. B., Eisenberg, P. D., Selaru, P., Wilner, K. D., et al. (2010) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-09-1920 · Cited by 237 · cited 1×
“A Phase II MEK inhibitor trial with PD0325901 showed little efficacy in advanced NSCLC; however, patients were not preselected by mutation statu”
Method
Amplification of EGFR T790M causes resistance to an irreversible EGFR inhibitor
Ercan, D., Zejnullahu, K., Yonesaka, K., Xiao, Y., Capelletti, M., Rogers, A. M., Lifshits, E., Brown, A., Lee, C., Christensen, J. G., et al. (2010) · Oncogene · doi:10.1038/onc.2009.526 · Cited by 235 · cited 1×
“In vitro , gefitinib-resistant cells already harbouring T790M further amplify the T790M allele on exposure to PF-0299804 (Ref”
Background
An integrated genomic analysis of lung cancer reveals loss of DUSP4 in EGFR-mutant tumors
Chitale, D. A., Gong, Y., Taylor, B. S., Broderick, S., Brennan, C., Somwar, R., Golas, B., Wang, L., Motoi, N., Szőke, J., et al. (2009) · Oncogene · doi:10.1038/onc.2009.135 · Cited by 232 · cited 1×
“Multiple genomic studies have shown that EGFR -mutant NSCLCs represent distinct disease phenotypes that have unique expression, mutation and copy number signature”
BackgroundSelf-citation
Oncogene Mutations, Copy Number Gains and Mutant Allele Specific Imbalance (MASI) Frequently Occur Together in Tumor Cells
Soh, J., Okumura, N., Lockwood, W. W., Yamamoto, H., Shigematsu, H., Zhang, W., Chari, R., Shames, D. S., Tang, X., MacAulay, C. E., et al. (2009) · PLoS ONE · doi:10.1371/journal.pone.0007464 · Cited by 227 · cited 1×
“EGFR mutations are usually heterozygous, with the mutant allele also showing gene amplificatio”
Background
Antitumor activity and pharmacokinetic properties of PF-00299804, a second-generation irreversible pan-erbB receptor tyrosine kinase inhibitor
Gonzales, A. J., Hook, K. E., Althaus, I. W., Ellis, P. A., Trachet, E., Delaney, A. M., Harvey, P. J., Ellis, T. A., Amato, D. M., Nelson, J. M., et al. (2008) · Molecular Cancer Therapeutics · doi:10.1158/1535-7163.mct-07-2232 · Cited by 226
Chemogenomic profiling provides insights into the limited activity of irreversible EGFR Inhibitors in tumor cells expressing the T790M EGFR resistance mutation.
Sos, M. L., Rode, H. B., Heynck, S., Peifer, M., Fischer, F., Klüter, S., Pawar, V. G., Reuter, C., Heuckmann, J. M., Weiss, J., et al. (2010) · Cancer Research · doi:10.1158/0008-5472.can-09-3106 · Cited by 220 · cited 1×
“This restoration closes the therapeutic window that is opened by the diminished ATP affinity of the oncogenic mutants, which are normally more easily inhibited relative to wild-type EGF”
Background
Epidermal Growth Factor Receptor Mutation Testing in Lung Cancer: Searching for the Ideal Method
Pao, W. J., & Ladanyi, M. (2007) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-07-1387 · Cited by 214 · cited 1×
“This observation can be partly explained by the fact that all molecular diagnostic tests for EGFR mutations have an inherent limit of detectio”
BackgroundSelf-citation
High dose weekly erlotinib achieves therapeutic concentrations in CSF and is effective in leptomeningeal metastases from epidermal growth factor receptor mutant lung cancer
Clarke, J. L., Pao, W., Wu, N., Miller, V. A., & Lassman, A. B. (2010) · Journal of Neuro-Oncology · doi:10.1007/s11060-010-0128-6 · Cited by 214 · cited 1×
“This observation may be due to a lack of selective pressure, as the concentration of EGFR TKI that reaches the brain is 100-fold less than that found in bloo”
BackgroundSelf-citation
The T790M “gatekeeper” mutation in EGFR mediates resistance to low concentrations of an irreversible EGFR inhibitor
Godin-Heymann, N., Ulkus, L., Brannigan, B. W., McDermott, U., Lamb, J. A., Maheswaran, S., Settleman, J. E., & Haber, D. A. (2008) · Molecular Cancer Therapeutics · doi:10.1158/1535-7163.mct-07-2387 · Cited by 209
Alterations in Genes of the EGFR Signaling Pathway and Their Relationship to EGFR Tyrosine Kinase Inhibitor Sensitivity in Lung Cancer Cell Lines
Gandhi, J., Zhang, J., Xie, Y., Soh, J., Shigematsu, H., Zhang, W., Yamamoto, H., Peyton, M., Girard, L., Lockwood, W. W., et al. (2009) · PLoS ONE · doi:10.1371/journal.pone.0004576 · Cited by 200 · cited 1×
“The two drugs are dosed differently (that is, erlotinib is administered at its maximum-tolerated dose whereas gefitinib is not); however, both EGFR inhibitors have similar, strongly correlated inhibitory patterns in EGFR -mutated cells in vitro”
Background
Analysis of epidermal growth factor receptor expression as a predictive factor for response to gefitinib (‘Iressa’, ZD1839) in non-small-cell lung cancer
Parra, H. J. S., Cavina, R., Latteri, F. S., Zucali, P. A., Campagnoli, E., Morenghi, E., Grimaldi, G. C., Roncalli, M. G., & Santoro, A. (2004) · British Journal of Cancer · doi:10.1038/sj.bjc.6601923 · Cited by 200
Bypassing cellular EGF receptor dependence through epithelial-to-mesenchymal-like transitions
Barr, S. M., Thomson, S., Buck, E. A., Russo, S. M., Petti, F., Sujka-Kwok, I., Eyzaguirre, A., Rosenfeld-Franklin, M., Gibson, N. W., Miglarese, M. R., et al. (2008) · Clinical & Experimental Metastasis · doi:10.1007/s10585-007-9121-7 · Cited by 199 · cited 1×
“The shift in signalling networks resulting from EMT may alleviate dependence on EGFR signallin”
Background
Emergence of Epidermal Growth Factor Receptor T790M Mutation during Chronic Exposure to Gefitinib in a Non–Small Cell Lung Cancer Cell Line
Ogino, A., Kitao, H., Hirano, S., Uchida, A., Ishiai, M., Kozuki, T., Takigawa, N., Takata, M., Kiura, K., & Tanimoto, M. (2007) · Cancer Research · doi:10.1158/0008-5472.can-07-0681 · Cited by 194
Epidermal Growth Factor Receptor Mutants from Human Lung Cancers Exhibit Enhanced Catalytic Activity and Increased Sensitivity to Gefitinib
Mulloy, R., Ferrand, A., Kim, Y., Sordella, R., Bell, D. W., Haber, D. A., Anderson, K. S., & Settleman, J. (2007) · Cancer Research · doi:10.1158/0008-5472.can-06-4293 · Cited by 192 · cited 1×
“Biochemical data further show enhanced kinase activity and transformation capabilities of EGFR in the presence of L858R or the exon 19 deletio”
Background
Epidermal Growth Factor Receptor Mutations in Small Cell Lung Cancer
Tatematsu, A., Shimizu, J., Murakami, Y., Horio, Y., Nakamura, S., Hida, T., Mitsudomi, T., & Yatabe, Y. (2008) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-08-0332 · Cited by 191
Telangiectatic osteogenic sarcoma
Matsuno, T., Unni, K. K., McLeod, R. A., & Dahlin, D. C. (1976) · Cancer · doi:10.1002/1097-0142(197612)38:6 · Cited by 184
Phase II Trial of Cetuximab in Patients With Previously Treated Non–Small-Cell Lung Cancer
Hanna, N. H., Lilenbaum, R., Ansari, R., Lynch, T. J., Govindan, R., Janne, P. A., & Bonomi, P. (2006) · Journal of Clinical Oncology · doi:10.1200/jco.2006.08.2263 · Cited by 184
ZD6474 – a novel inhibitor of VEGFR and EGFR tyrosine kinase activity
Ryan, A. J., & Wedge, S. R. (2005) · British Journal of Cancer · doi:10.1038/sj.bjc.6602603 · Cited by 178
Effects of Erlotinib in EGFR Mutated Non-Small Cell Lung Cancers with Resistance to Gefitinib
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., et al. (2008) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-08-1455 · Cited by 171
Self-citation
Epithelial-mesenchymal transition in EGFR-TKI acquired resistant lung adenocarcinoma.
Uramoto, H., Iwata, T., Onitsuka, T., Shimokawa, H., Hanagiri, T., & Oyama, T. (2010) · PubMed · Cited by 168
Proapoptotic BH3-Only BCL-2 Family Protein BIM Connects Death Signaling from Epidermal Growth Factor Receptor Inhibition to the Mitochondrion
Deng, J., Shimamura, T., Perera, S. A., Carlson, N. E., Cai, D. D., Shapiro, G. I., Wong, K., & Letai, A. G. (2007) · Cancer Research · doi:10.1158/0008-5472.can-07-1961 · Cited by 160
Oncogenic Activity of Epidermal Growth Factor Receptor Kinase Mutant Alleles Is Enhanced by the T790M Drug Resistance Mutation
Godin-Heymann, N., Bryant, I., Rivera, M. N., Ulkus, L., Bell, D. W., Riese, D. J., Settleman, J. E., & Haber, D. A. (2007) · Cancer Research · doi:10.1158/0008-5472.can-06-4625 · Cited by 157
Phase I Study of EKB-569, an Irreversible Inhibitor of the Epidermal Growth Factor Receptor, in Patients With Advanced Solid Tumors
Erlichman, C., Hidalgo, M. M., Boni, J. P., Martins, P., Quinn, S., Zacharchuk, C., Amorusi, P., Adjei, A. A., & Rowinsky, E. K. (2006) · Journal of Clinical Oncology · doi:10.1200/jco.2005.01.8960 · Cited by 149
Mect1-Maml2 fusion oncogene linked to the aberrant activation of cyclic AMP/CREB regulated genes.
Coxon, A., Rozenblum, E., Park, Y., Joshi, N., Tsurutani, J., Dennis, P., Kirsch, I., & Kaye, F. (2005) · Cancer Research · doi:10.1158/0008-5472.can-05-1125 · Cited by 144 · cited 1×
“, and MEC cell lines are sensitive to EGFR TKIs in vitro”
Background
High Expression Levels of Total IGF-1R and Sensitivity of NSCLC Cells In Vitro to an Anti-IGF-1R Antibody (R1507)
Gong, Y., Yao, E. S., Shen, R., Goel, A. J., Arcila, M. E., Teruya‐Feldstein, J., Zakowski, M. F., Frankel, S., Peifer, M., Thomas, R. K., et al. (2009) · PLoS ONE · doi:10.1371/journal.pone.0007273 · Cited by 131
Self-citation
Differential Responses to Erlotinib in Epidermal Growth Factor Receptor (EGFR)-Mutated Lung Cancers With Acquired Resistance to Gefitinib Carrying the L747S or T790M Secondary Mutations
Costa, D. B., Schumer, S., Tenen, D. G., & Kobayashi, S. S. (2008) · Journal of Clinical Oncology · doi:10.1200/jco.2007.14.9039 · Cited by 126 · cited 1×
“Three other second-site mutations in EGFR have been associated with acquired resistance, including L747S (exon 19”
Background
Sequential occurrence of non-small cell and small cell lung cancer with the same EGFR mutation
Morinaga, R., Okamoto, I., Furuta, K., Kawano, Y., Sekijima, M., Dote, K., Satou, T., Nishio, K., Fukuoka, M., & Nakagawa, K. (2007) · Lung Cancer · doi:10.1016/j.lungcan.2007.05.014 · Cited by 116
Evolution of Resistance to Targeted Anti-Cancer Therapies during Continuous and Pulsed Administration Strategies
Foo, J., & Michor, F. (2009) · PLoS Computational Biology · doi:10.1371/journal.pcbi.1000557 · Cited by 114
The phosphatase and tensin homolog regulates epidermal growth factor receptor (EGFR) inhibitor response by targeting EGFR for degradation
Vivanco, I., Rohle, D., Versele, M., Iwanami, A., Kuga, D., Oldrini, B., Tanaka, K., Dang, J. H. T., Kubek, S., Palaskas, N. J., et al. (2010) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0911188107 · Cited by 108
Effect of re-treatment with gefitinib (‘Iressa’, ZD1839) after acquisition of resistance
Kurata, T., Tamura, K., Kaneda, H., Nogami, T., Uejima, H., Asai, G., Nakagawa, K., & Fukuoka, M. (2003) · Annals of Oncology · doi:10.1093/annonc/mdh006 · Cited by 107 · cited 1×
“, multiple re-responses to EGFR TKIs following a short hiatus without targeted therapy have been reporte”
Background
EGFR-T790M Is a Rare Lung Cancer Susceptibility Allele with Enhanced Kinase Activity
Vikis, H. G., Sato, M., James, M. A., Wang, D., Wang, Y., Wang, M., Jia, D., Liu, Y., Wilson, J., Amos, C. I., et al. (2007) · Cancer Research · doi:10.1158/0008-5472.can-07-0217 · Cited by 106
Mucoepidermoid carcinoma of lung: Potential target of EGFR-directed treatment
Han, S., Kim, H., Jeon, Y. K., Oh, D., Lee, S., Kim, D., Im, S., Chung, D. H., Heo, D. S., Bang, Y., et al. (2008) · Lung Cancer · doi:10.1016/j.lungcan.2007.11.014 · Cited by 103
Retreatment of Lung Adenocarcinoma Patients With Gefitinib Who Had Experienced Favorable Results From Their Initial Treatment With This Selective Epidermal Growth Factor Receptor Inhibitor: A Report of Three Cases
Yano, S., Nakataki, E., Ohtsuka, S., Inayama, M., Tomimoto, H., Edakuni, N., Kakiuchi, S., Nishikubo, N., Muguruma, H., & Sone, S. (2005) · Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics · doi:10.3727/096504005775082020 · Cited by 99
CI-1033, an irreversible pan-erbB receptor inhibitor and its potential application for the treatment of breast cancer
Allen, L. F. (2003) · Seminars in Oncology · doi:10.1053/j.seminoncol.2003.08.009 · Cited by 99
Analysis of Genetic Variants in Never-Smokers with Lung Cancer Facilitated by an Internet-Based Blood Collection Protocol: A Preliminary Report
Girard, N., Lou, E., Azzoli, C. G., Reddy, R., Robson, M. E., Harlan, M., Orlow, I., Yatabe, Y., Nafa, K., Ladanyi, M., et al. (2010) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-09-2437 · Cited by 94
Self-citation
The Insulin-Like Growth Factor Pathway in Lung Cancer
Dziadziuszko, R., Camidge, D. R., & Hirsch, F. R. (2008) · Journal of Thoracic Oncology · doi:10.1097/jto.0b013e31818180f5 · Cited by 90 · cited 1×
“, addition of a GF1R-specific antibody (reviewed in Ref”
Background
Inhibition of the T790M Gatekeeper Mutant of the Epidermal Growth Factor Receptor by EXEL-7647
Gendreau, S. B., Ventura, R., Keast, P., Laird, A., Yakes, F. M., Zhang, W., Bentzien, F., Cancilla, B., Lutman, J., Chu, F., et al. (2007) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-06-2590 · Cited by 90
Comparison of the EGFR resistance mutation profiles generated by EGFR-targeted tyrosine kinase inhibitors and the impact of drug combinations
Avizienyte, E., Ward, R. A., & Garner, A. P. (2008) · Biochemical Journal · doi:10.1042/bj20080728 · Cited by 88
Erlotinib resistance in mouse models of epidermal growth factor receptor-induced lung adenocarcinoma
Politi, K. A., Fan, P., Shen, R., Zakowski, M. F., & VARMUS, H. E. (2009) · Disease Models & Mechanisms · doi:10.1242/dmm.003681 · Cited by 86 · cited 1×
“One promising approach involves the study of acquired resistance in mouse models of EGFR TKI-sensitive lung tumour”
Background
Erlotinib at a Dose of 25 mg Daily for Non-small Cell Lung Cancers with EGFR Mutations
Yeo, W.-L., Riely, G. J., Yeap, B. Y., Lau, M. W., Warner, J. L., Bodio, K., Huberman, M. S., Kris, M. G., Tenen, D. G., Pao, W. J., et al. (2010) · Journal of Thoracic Oncology · doi:10.1097/jto.0b013e3181dd1386 · Cited by 82 · cited 1×
“The two drugs are dosed differently (that is, erlotinib is administered at its maximum-tolerated dose whereas gefitinib is not); however, both EGFR inhibitors have similar, strongly correlated inhibitory patterns in EGFR -mutated cells in vitro”
BackgroundSelf-citation
Double EGFR mutants containing rare EGFR mutant types show reduced in vitro response to gefitinib compared with common activating missense mutations
Tam, I. Y. S., Leung, E. L., Tin, V. P., Chua, D. T.-T., Sihoe, A. D., Cheng, L., Chung, L.-P., & Wong, M. P. (2009) · Molecular Cancer Therapeutics · doi:10.1158/1535-7163.mct-08-1219 · Cited by 76 · cited 1×
“In vitro , the double-mutant receptor has been shown to be less sensitive to EGFR drugs than the G719C mutant alon”
Background
Preliminary activity and safety results from a phase I clinical trial of PF-00299804, an irreversible pan-HER inhibitor, in patients (pts) with NSCLC
Janne, P. A., Schellens, J. H. M., Engelman, J. A., Eckhardt, S. G., Millham, R., Denis, L. J., Britten, C. D., Wong, S. G., Boss, D. S., & Camidge, D. R. (2008) · Journal of Clinical Oncology · doi:10.1200/jco.2008.26.15_suppl.8027 · Cited by 67
Gefitinib as targeted therapy for mucoepidermoid carcinoma of the lung: Possible significance of CRTC1–MAML2 oncogene
O’Neill, I. D. (2009) · Lung Cancer · doi:10.1016/j.lungcan.2009.01.003 · Cited by 53
Germ-Line and Somatic Presentations of the EGFR T790M Mutation in Lung Cancer
Prudkin, L., Tang, X., & Wistuba, I. I. (2009) · Journal of Thoracic Oncology · doi:10.1097/jto.0b013e3181915f92 · Cited by 52
Epidermal growth factor receptor tyrosine kinase inhibitors as first-line treatment in advanced nonsmall-cell lung cancer
Rosell, R., Viteri, S., Molina‐Vila, M. Á., Benlloch, S., & Tarón, M. (2010) · Current Opinion in Oncology · doi:10.1097/cco.0b013e32833500d2 · Cited by 45 · cited 1×
“Finally, similar response, PFS and survival rates have been observed for erlotinib and gefitini”
Background
Differences underlying EGFR and HER2 oncogene addiction
Faber, A. C., Wong, K., & Engelman, J. A. (2010) · Cell Cycle · doi:10.4161/cc.9.5.11096 · Cited by 41
Living With Imperfection
Mok, T. S. K. (2009) · Journal of Clinical Oncology · doi:10.1200/jco.2009.25.8574 · Cited by 34 · cited 1×
“However, despite this enhanced oncogenicity of T790M-harbouring EGFR, patients with this form of acquired resistance can display slow rates of disease progressio”
Background
Chemotherapy of Advanced Non-Small Cell Lung Cancer
Pirker, R., & Minar, W. (2009) · Frontiers of radiation therapy and oncology · doi:10.1159/000262471 · Cited by 17
Molecular On/Off Switch
Milton, D. T., Riely, G. J., Pao, W. J., Miller, V. A., Kris, M. G., & Heelan, R. T. (2006) · Journal of Clinical Oncology · doi:10.1200/jco.2006.06.4410 · Cited by 11 · cited 1×
“, multiple re-responses to EGFR TKIs following a short hiatus without targeted therapy have been reporte”
BackgroundSelf-citation

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Oh, I.-J. et al. in AACR–IASLC Joint Conference on Molecular Origins of Lung Cancer: Prospects for Personalized Prevention and Therapy (Coronado, California USA, 2010).

Sorted by citations

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
Rosell, R., Carcereny, E., Gervais, R., Vergnenegre, A., Massuti, B., Felip, E., Palmero, R., Garcia-Gomez, R., Pallares, C., Sanchez, J. M., et al. (2012) · The Lancet Oncology · doi:10.1016/s1470-2045(11)70393-x · Cited by 5,489
The causes and consequences of genetic heterogeneity in cancer evolution
Burrell, R. A., McGranahan, N., Bartek, J., & Swanton, C. (2013) · Nature · doi:10.1038/nature12625 · Cited by 2,262
AZD9291, an Irreversible EGFR TKI, Overcomes T790M-Mediated Resistance to EGFR Inhibitors in Lung Cancer
Cross, D. A. E., Ashton, S. E., Ghiorghiu, S., Eberlein, C., Nebhan, C. A., Spitzler, P. J., Orme, J. P., Finlay, M. R. V., Ward, R. A., Mellor, M. J., et al. (2014) · Cancer Discovery · doi:10.1158/2159-8290.cd-14-0337 · Cited by 2,246
“Mutations in EGFR occur in 10% to 35% of NSCLCs and confer sensitivity to the EGFR TKIs erlotinib, gefitinib, and afatinib (6).”
InfluentialSelf-citation
Mapping the Hallmarks of Lung Adenocarcinoma with Massively Parallel Sequencing
Imielinski, M., Berger, A. H., Hammerman, P. S., Hernandez, B., Pugh, T. J., Hodis, E., Cho, J., Suh, J., Capelletti, M., Sivachenko, A., et al. (2012) · Cell · doi:10.1016/j.cell.2012.08.029 · Cited by 1,789
“…routinely used to guide clinical care of lung adenocarcinoma patients, largely due to clinical trials that demonstrated superior efficacy of targeted kinase inhibitors as compared to standard chemotherapy for patients with EGFR mutations or ALK fusions (Kwak et al., 2010; Pao and Chmielecki, 2010).”
BackgroundSelf-citation
Integrative genome analyses identify key somatic driver mutations of small-cell lung cancer
Peifer, M., Fernandez‐Cuesta, L., Sos, M. L., George, J., Seidel, D., Kasper, L. H., Plenker, D., Leenders, F., Sun, R., Zander, T., et al. (2012) · Nature Genetics · doi:10.1038/ng.2396 · Cited by 1,404
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Authors: Pao, W., & Chmielecki, J.
Affiliations: Vanderbilt University (US)
Corresponding author: Pao, William
ORCID: Pao, William
Chmielecki, Juliann
Venue: Nature Reviews Cancer
Publisher: Springer Science and Business Media LLC
Published: 2010-10-22
Volume: 10
Issue: 11
Pages: 760-774
ISSN: 1474-175X (ISSN-L)
1474-1768
DOI: 10.1038/nrc2947
PMC: PMC3072803
OpenAlex: W2090029719
Cited by: 1,083
References: 180
Citations by year: 2026: 24 · 2025: 43 · 2024: 54 · 2023: 49 · 2022: 45 · 2021: 65 · 2020: 79 · 2019: 56 · 2018: 69 · 2017: 72 · 2016: 90 · 2015: 82 · 2014: 93 · 2013: 93 · 2012: 104
FWCI: 14.65
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.springer.com/tdm (tdm)
Locations: Nature reviews. Cancer (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: Vanderbilt University
National Institutes of Health
University of California, San Francisco
National Cancer Institute (P30 CA 68485, R01CA121210, P01CA129243, CA90949, U54CA143798, P50CA090949, P30CA068485)
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-mutant non-small cell lung cancer, epidermal growth factor receptor, tyrosine kinase inhibitors, gefitinib, erlotinib, acquired drug resistance, primary resistance, targeted therapy
MeSH terms: Antineoplastic Agents, Carcinoma, Non-Small-Cell Lung, Humans, Lung Neoplasms, Mutation, Protein-Tyrosine Kinases, Drug Resistance, Neoplasm, Protein Kinase Inhibitors, ErbB Receptors

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Rational, biologically based treatment of EGFR-mutant non-small-cell lung cancer

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