Abstract

The timely discovery of cancer cell resistance in clinical processing and the accurate calculation of drug dosage to reduce and inhibit tumour growth factor in cancer patients are promising technologies in cancer therapy. Here, an optofluidic resonator effectively detects drug interactions with cancer cell processing in real time and enables the calculation of label-free drug-non-small cell lung cancer (NSCLC) epidermal growth factor receptor (EGFR) and binding ratios using molecular fluorescence intensity. According to clinical test and in vivo experimental data, the efficiencies of gefitinib and erlotinib are only 37% and 12% compared to AZD9291, and 0.300 μg of EGFR inactivation requires 0.484 μg of AZD9291, 0.815 μg of gefitinib and 1.348 μg of erlotinib. Experimental results show that the present method allows for the performance detection of drug resistance and for the evaluation of dosage usage.

© 2018 Optical Society of America under the terms of the OSA Open Access Publishing Agreement

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2017 (1)

K. Heinzmann, L. M. Carter, J. S. Lewis, and E. O. Absagye, “Multiplexed imaging for diagnosis and therapy,” Nature Biomedical Engineering 1(9), 697–713 (2017).
[Crossref]

2016 (1)

H. Dai, Z. Cao, Y. Wang, H. Li, M. Sang, W. Yuan, F. Chen, and X. Chen, “Concentric circular grating generated by the patterning trapping of nanoparticles in an optofluidic chip,” Sci. Rep. 6(1), 32018–32025 (2016).
[Crossref] [PubMed]

2014 (1)

E. C. de Bruin, C. Cowell, P. H. Warne, M. Jiang, R. E. Saunders, M. A. Melnick, S. Gettinger, Z. Walther, A. Wurtz, G. J. Heynen, D. A. Heideman, J. Gómez-Román, A. García-Castaño, Y. Gong, M. Ladanyi, H. Varmus, R. Bernards, E. F. Smit, K. Politi, and J. Downward, “Reduced NF1 expression confers resistance to EGFR inhibition in lung cancer,” Cancer Discov. 4(5), 606–619 (2014).
[Crossref] [PubMed]

2013 (1)

2012 (5)

M. J. Garnett, E. J. Edelman, S. J. Heidorn, C. D. Greenman, A. Dastur, K. W. Lau, P. Greninger, I. R. Thompson, X. Luo, J. Soares, Q. Liu, F. Iorio, D. Surdez, L. Chen, R. J. Milano, G. R. Bignell, A. T. Tam, H. Davies, J. A. Stevenson, S. Barthorpe, S. R. Lutz, F. Kogera, K. Lawrence, A. McLaren-Douglas, X. Mitropoulos, T. Mironenko, H. Thi, L. Richardson, W. Zhou, F. Jewitt, T. Zhang, P. O’Brien, J. L. Boisvert, S. Price, W. Hur, W. Yang, X. Deng, A. Butler, H. G. Choi, J. W. Chang, J. Baselga, I. Stamenkovic, J. A. Engelman, S. V. Sharma, O. Delattre, J. Saez-Rodriguez, N. S. Gray, J. Settleman, P. A. Futreal, D. A. Haber, M. R. Stratton, S. Ramaswamy, U. McDermott, and C. H. Benes, “Systematic identification of genomic markers of drug sensitivity in cancer cells,” Nature 483(7391), 570–575 (2012).
[Crossref] [PubMed]

K. Ohashi, L. V. Sequist, M. E. Arcila, T. Moran, J. Chmielecki, Y. L. Lin, Y. Pan, L. Wang, E. de Stanchina, K. Shien, K. Aoe, S. Toyooka, K. Kiura, L. Fernandez-Cuesta, P. Fidias, J. C. Yang, V. A. Miller, G. J. Riely, M. G. Kris, J. A. Engelman, C. L. Vnencak-Jones, D. Dias-Santagata, M. Ladanyi, and W. Pao, “Lung cancers with acquired resistance to EGFR inhibitors occasionally harbor BRAF gene mutations but lack mutations in KRAS, NRAS, or MEK1,” Proc. Natl. Acad. Sci. U.S.A. 109(31), E2127–E2133 (2012).
[Crossref] [PubMed]

S. S. Ramalingam, F. Blackhall, M. Krzakowski, C. H. Barrios, K. Park, I. Bover, D. Seog Heo, R. Rosell, D. C. Talbot, R. Frank, S. P. Letrent, A. Ruiz-Garcia, I. Taylor, J. Q. Liang, A. K. Campbell, J. O’Connell, and M. Boyer, “Randomized phase II study of dacomitinib (PF-00299804), an irreversible pan-human epidermal growth factor receptor inhibitor, versus erlotinib in patients with advanced non-small-cell lung cancer,” J. Clin. Oncol. 30(27), 3337–3344 (2012).
[Crossref] [PubMed]

R. Rosell, E. Carcereny, R. Gervais, A. Vergnenegre, B. Massuti, E. Felip, R. Palmero, R. Garcia-Gomez, C. Pallares, J. M. Sanchez, R. Porta, M. Cobo, P. Garrido, F. Longo, T. Moran, A. Insa, F. De Marinis, R. Corre, I. Bover, A. Illiano, E. Dansin, J. de Castro, M. Milella, N. Reguart, G. Altavilla, U. Jimenez, M. Provencio, M. A. Moreno, J. Terrasa, J. Muñoz-Langa, J. Valdivia, D. Isla, M. Domine, O. Molinier, J. Mazieres, N. Baize, R. Garcia-Campelo, G. Robinet, D. Rodriguez-Abreu, G. Lopez-Vivanco, V. Gebbia, L. Ferrera-Delgado, P. Bombaron, R. Bernabe, A. Bearz, A. Artal, E. Cortesi, C. Rolfo, M. Sanchez-Ronco, A. Drozdowskyj, C. Queralt, I. de Aguirre, J. L. Ramirez, J. J. Sanchez, M. A. Molina, M. Taron, and L. Paz-Ares, “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,” Lancet Oncol. 13(3), 239–246 (2012).
[Crossref] [PubMed]

K. Takezawa, V. Pirazzoli, M. E. Arcila, C. A. Nebhan, X. Song, E. de Stanchina, K. Ohashi, Y. Y. Janjigian, P. J. Spitzler, M. A. Melnick, G. J. Riely, M. G. Kris, V. A. Miller, M. Ladanyi, K. Politi, and W. Pao, “HER2 amplification: a potential mechanism of acquired resistance to EGFR inhibition in EGFR-mutant lung cancers that lack the second-site EGFRT790M mutation,” Cancer Discov. 2(10), 922–933 (2012).
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L. V. Sequist, B. A. Waltman, D. Dias-Santagata, S. Digumarthy, A. B. Turke, P. Fidias, K. Bergethon, A. T. Shaw, S. Gettinger, A. K. Cosper, S. Akhavanfard, R. S. Heist, J. Temel, J. G. Christensen, J. C. Wain, T. J. Lynch, K. Vernovsky, E. J. Mark, M. Lanuti, A. J. Iafrate, M. Mino-Kenudson, and J. A. Engelman, “Genotypic and histological evolution of lung cancers acquiring resistance to EGFR inhibitors,” Sci. Transl. Med. 3(75), 75ra26 (2011).
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X. Fan and I. M. White, “Optofluidic microsystems for chemical and biological analysis,” Nat. Photonics 5(10), 591–597 (2011).
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W. Yuan, C. Yin, H. Li, P. Xiao, and Z. Cao, “Wideband slow light assisted by ultrahigh-order modes,” J.O.S.A.B 28(5), 968–971 (2011).
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2010 (5)

M. L. Sos, H. B. Rode, S. Heynck, M. Peifer, F. Fischer, S. Klüter, V. G. Pawar, C. Reuter, J. M. Heuckmann, J. Weiss, L. Ruddigkeit, M. Rabiller, M. Koker, J. R. Simard, M. Getlik, Y. Yuza, T. H. Chen, H. Greulich, R. K. Thomas, and D. Rauh, “Chemogenomic profiling provides insights into the limited activity of irreversible EGFR Inhibitors in tumor cells expressing the T790M EGFR resistance mutation,” Cancer Res. 70(3), 868–874 (2010).
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K. E. Ware, M. E. Marshall, L. R. Heasley, L. Marek, T. K. Hinz, P. Hercule, B. A. Helfrich, R. C. Doebele, and L. E. Heasley, “Rapidly acquired resistance to EGFR tyrosine kinase inhibitors in NSCLC cell lines through de-repression of FGFR2 and FGFR3 expression,” PLoS One 5(11), e14117 (2010).
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W. Pao and J. Chmielecki, “Rational, biologically based treatment of EGFR-mutant non-small-cell lung cancer,” Nat. Rev. Cancer 10(11), 760–774 (2010).
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M. Maemondo, A. Inoue, K. Kobayashi, S. Sugawara, S. Oizumi, H. Isobe, A. Gemma, M. Harada, H. Yoshizawa, I. Kinoshita, Y. Fujita, S. Okinaga, H. Hirano, K. Yoshimori, T. Harada, T. Ogura, M. Ando, H. Miyazawa, M. S. T. Tanaka, Y. Saijo, K. Hagiwara, S. Morita, and T. Nukiwa, “Geftinib or chemotherapy for non-small-cell lung cancer with mutated EGFR,” N. Engl. J. Med. 362, 2380–2388 (2010).

T. Mitsudomi, S. Morita, Y. Yatabe, S. Negoro, I. Okamoto, J. Tsurutani, T. Seto, M. Satouchi, H. Tada, T. Hirashima, K. Asami, N. Katakami, M. Takada, H. Yoshioka, K. Shibata, S. Kudoh, E. Shimizu, H. Saito, S. Toyooka, K. Nakagawa, and M. Fukuoka, “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,” Lancet Oncol. 11(2), 121–128 (2010).
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2009 (2)

T. S. Mok, Y. L. Wu, S. Thongprasert, C. H. Yang, D. T. Chu, N. Saijo, P. Sunpaweravong, B. Han, B. Margono, Y. Ichinose, Y. Nishiwaki, Y. Ohe, J. J. Yang, B. Chewaskulyong, H. Jiang, E. L. Duffield, C. L. Watkins, A. A. Armour, and M. Fukuoka, “Gefitinib or carboplatin-paclitaxel in pulmonary adenocarcinoma,” N. Engl. J. Med. 361(10), 947–957 (2009).
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B. Burtness, M. Anadkat, S. Basti, M. Hughes, M. E. Lacouture, J. S. McClure, P. L. Myskowski, J. Paul, C. S. Perlis, L. Saltz, and S. Spencer, “NCCN Task Force Report: Management of dermatologic and other toxicities associated with EGFR inhibition in patients with cancer,” J. Natl. Compr. Canc. Netw. 7(1), S5–S21, quiz S22–S24 (2009).
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2008 (5)

C. H. Yun, K. E. Mengwasser, A. V. Toms, M. S. Woo, H. Greulich, K. K. Wong, M. Meyerson, and M. J. Eck, “The T790M mutation in EGFR kinase causes drug resistance by increasing the affinity for ATP,” Proc. Natl. Acad. Sci. U.S.A. 105(6), 2070–2075 (2008).
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D. Li, L. Ambrogio, T. Shimamura, S. Kubo, M. Takahashi, L. R. Chirieac, R. F. Padera, G. I. Shapiro, A. Baum, F. Himmelsbach, W. J. Rettig, M. Meyerson, F. Solca, H. Greulich, and K. K. Wong, “BIBW2992, an irreversible EGFR/HER2 inhibitor highly effective in preclinical lung cancer models,” Oncogene 27(34), 4702–4711 (2008).
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Y. Wang, Z. Cao, T. Yu, H. Li, and Q. Shen, “Enhancement of the superprism effect based on the strong dispersion effect of ultrahigh-order modes,” Opt. Lett. 33(11), 1276–1278 (2008).
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X. Fan, I. M. White, S. I. Shopova, H. Zhu, J. D. Suter, and Y. Sun, “Sensitive optical biosensors for unlabeled targets: a review,” Anal. Chim. Acta 620(1-2), 8–26 (2008).
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J. Homola, “Surface plasmon resonance sensors for detection of chemical and biological species,” Chem. Rev. 108(2), 462–493 (2008).
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2007 (4)

C. H. Yun, T. J. Boggon, Y. Li, M. S. Woo, H. Greulich, M. Meyerson, and M. J. Eck, “Structures of lung cancer-derived EGFR mutants and inhibitor complexes: mechanism of activation and insights into differential inhibitor sensitivity,” Cancer Cell 11(3), 217–227 (2007).
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J. A. Engelman, K. Zejnullahu, C. M. Gale, E. Lifshits, A. J. Gonzales, T. Shimamura, F. Zhao, P. W. Vincent, G. N. Naumov, J. E. Bradner, I. W. Althaus, L. Gandhi, G. I. Shapiro, J. M. Nelson, J. V. Heymach, M. Meyerson, K. K. Wong, and P. A. Jänne, “PF00299804, an irreversible pan-ERBB inhibitor, is effective in lung cancer models with EGFR and ERBB2 mutations that are resistant to gefitinib,” Cancer Res. 67(24), 11924–11932 (2007).
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J. Bean, C. Brennan, J. Y. Shih, G. Riely, A. Viale, L. Wang, D. Chitale, N. Motoi, J. Szoke, S. Broderick, M. Balak, W. C. Chang, C. J. Yu, A. Gazdar, H. Pass, V. Rusch, W. Gerald, S. F. Huang, P. C. Yang, V. Miller, M. Ladanyi, C. H. Yang, and W. Pao, “MET amplification occurs with or without T790M mutations in EGFR mutant lung tumors with acquired resistance to gefitinib or erlotinib,” Proc. Natl. Acad. Sci. U.S.A. 104(52), 20932–20937 (2007).
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J. A. Engelman, K. Zejnullahu, T. Mitsudomi, Y. Song, C. Hyland, J. O. Park, N. Lindeman, C. M. Gale, X. Zhao, J. Christensen, T. Kosaka, A. J. Holmes, A. M. Rogers, F. Cappuzzo, T. Mok, C. Lee, B. E. Johnson, L. C. Cantley, and P. A. Jänne, “MET amplification leads to gefitinib resistance in lung cancer by activating ERBB3 signaling,” Science 316(5827), 1039–1043 (2007).
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2005 (2)

S. Kobayashi, T. J. Boggon, T. Dayaram, P. A. Jänne, O. Kocher, M. Meyerson, B. E. Johnson, M. J. Eck, D. G. Tenen, and B. Halmos, “EGFR mutation and resistance of non-small-cell lung cancer to gefitinib,” N. Engl. J. Med. 352(8), 786–792 (2005).
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W. Pao, V. A. Miller, K. A. Politi, G. J. Riely, R. Somwar, M. F. Zakowski, M. G. Kris, and H. Varmus, “Acquired resistance of lung adenocarcinomas to gefitinib or erlotinib is associated with a second mutation in the EGFR kinase domain,” PLoS Med. 2(3), e73 (2005).
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2004 (4)

T. J. Lynch, D. W. Bell, R. Sordella, S. Gurubhagavatula, R. A. Okimoto, B. W. Brannigan, P. L. Harris, S. M. Haserlat, J. G. Supko, F. G. Haluska, D. N. Louis, D. C. Christiani, J. Settleman, and D. A. Haber, “Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib,” N. Engl. J. Med. 350(21), 2129–2139 (2004).
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J. Guillermo Paez, P. Pasi Janne, J. C. Lee, S. Tracy, H. Greulich, S. Gabriel, P. Herman, F. J. Kaye, N. Lindeman, T. J. Boggon, K. Naoki, H. Sasaki, Y. Fujii, M. J. Eck, W. R. Sellers, B. E. Johnson, and M. Meyerson, “EGFR mutations in lung cancer: correlation with clinical response to geftinib therapy,” Science 304, 1497–1500 (2004).
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W. Pao, V. Miller, M. Zakowski, J. Doherty, K. Politi, I. Sarkaria, B. Singh, R. Heelan, V. Rusch, L. Fulton, E. Mardis, D. Kupfer, R. Wilson, M. Kris, and H. Varmus, “EGF receptor gene mutations are common in lung cancers from “never smokers” and are associated with sensitivity of tumors to gefitinib and erlotinib,” Proc. Natl. Acad. Sci. U.S.A. 101(36), 13306–13311 (2004).
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P. Andrew and W. L. Barnes, “Energy transfer across a metal film mediated by surface plasmon polaritons,” Science 306(5698), 1002–1005 (2004).
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2002 (1)

R. Horvath, H. C. Pedersen, and N. B. Larsen, “Demonstration of reverse symmetry waveguide sensing in aqueous solutions,” Appl. Phys. Lett. 81(12), 2166–2168 (2002).
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2001 (1)

A. J. Barker, K. H. Gibson, W. Grundy, A. A. Godfrey, J. J. Barlow, M. P. Healy, J. R. Woodburn, S. E. Ashton, B. J. Curry, L. Scarlett, L. Henthorn, and L. Richards, “Studies leading to the identification of ZD1839 (IRESSA): an orally active, selective epidermal growth factor receptor tyrosine kinase inhibitor targeted to the treatment of cancer,” Bioorg. Med. Chem. Lett. 11(14), 1911–1914 (2001).
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2000 (1)

Y. Sako, S. Minoghchi, and T. Yanagida, “Single-molecule imaging of EGFR signalling on the surface of living cells,” Nat. Cell Biol. 2(3), 168–172 (2000).
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1997 (1)

J. D. Moyer, E. G. Barbacci, K. K. Iwata, L. Arnold, B. Boman, A. Cunningham, C. DiOrio, J. Doty, M. J. Morin, M. P. Moyer, M. Neveu, V. A. Pollack, L. R. Pustilnik, M. M. Reynolds, D. Sloan, A. Theleman, and P. Miller, “Induction of apoptosis and cell cycle arrest by CP-358,774, an inhibitor of epidermal growth factor receptor tyrosine kinase,” Cancer Res. 57(21), 4838–4848 (1997).
[PubMed]

Absagye, E. O.

K. Heinzmann, L. M. Carter, J. S. Lewis, and E. O. Absagye, “Multiplexed imaging for diagnosis and therapy,” Nature Biomedical Engineering 1(9), 697–713 (2017).
[Crossref]

Akhavanfard, S.

L. V. Sequist, B. A. Waltman, D. Dias-Santagata, S. Digumarthy, A. B. Turke, P. Fidias, K. Bergethon, A. T. Shaw, S. Gettinger, A. K. Cosper, S. Akhavanfard, R. S. Heist, J. Temel, J. G. Christensen, J. C. Wain, T. J. Lynch, K. Vernovsky, E. J. Mark, M. Lanuti, A. J. Iafrate, M. Mino-Kenudson, and J. A. Engelman, “Genotypic and histological evolution of lung cancers acquiring resistance to EGFR inhibitors,” Sci. Transl. Med. 3(75), 75ra26 (2011).
[Crossref] [PubMed]

Altavilla, G.

R. Rosell, E. Carcereny, R. Gervais, A. Vergnenegre, B. Massuti, E. Felip, R. Palmero, R. Garcia-Gomez, C. Pallares, J. M. Sanchez, R. Porta, M. Cobo, P. Garrido, F. Longo, T. Moran, A. Insa, F. De Marinis, R. Corre, I. Bover, A. Illiano, E. Dansin, J. de Castro, M. Milella, N. Reguart, G. Altavilla, U. Jimenez, M. Provencio, M. A. Moreno, J. Terrasa, J. Muñoz-Langa, J. Valdivia, D. Isla, M. Domine, O. Molinier, J. Mazieres, N. Baize, R. Garcia-Campelo, G. Robinet, D. Rodriguez-Abreu, G. Lopez-Vivanco, V. Gebbia, L. Ferrera-Delgado, P. Bombaron, R. Bernabe, A. Bearz, A. Artal, E. Cortesi, C. Rolfo, M. Sanchez-Ronco, A. Drozdowskyj, C. Queralt, I. de Aguirre, J. L. Ramirez, J. J. Sanchez, M. A. Molina, M. Taron, and L. Paz-Ares, “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,” Lancet Oncol. 13(3), 239–246 (2012).
[Crossref] [PubMed]

Althaus, I. W.

J. A. Engelman, K. Zejnullahu, C. M. Gale, E. Lifshits, A. J. Gonzales, T. Shimamura, F. Zhao, P. W. Vincent, G. N. Naumov, J. E. Bradner, I. W. Althaus, L. Gandhi, G. I. Shapiro, J. M. Nelson, J. V. Heymach, M. Meyerson, K. K. Wong, and P. A. Jänne, “PF00299804, an irreversible pan-ERBB inhibitor, is effective in lung cancer models with EGFR and ERBB2 mutations that are resistant to gefitinib,” Cancer Res. 67(24), 11924–11932 (2007).
[Crossref] [PubMed]

Ambrogio, L.

D. Li, L. Ambrogio, T. Shimamura, S. Kubo, M. Takahashi, L. R. Chirieac, R. F. Padera, G. I. Shapiro, A. Baum, F. Himmelsbach, W. J. Rettig, M. Meyerson, F. Solca, H. Greulich, and K. K. Wong, “BIBW2992, an irreversible EGFR/HER2 inhibitor highly effective in preclinical lung cancer models,” Oncogene 27(34), 4702–4711 (2008).
[Crossref] [PubMed]

Anadkat, M.

B. Burtness, M. Anadkat, S. Basti, M. Hughes, M. E. Lacouture, J. S. McClure, P. L. Myskowski, J. Paul, C. S. Perlis, L. Saltz, and S. Spencer, “NCCN Task Force Report: Management of dermatologic and other toxicities associated with EGFR inhibition in patients with cancer,” J. Natl. Compr. Canc. Netw. 7(1), S5–S21, quiz S22–S24 (2009).
[Crossref] [PubMed]

Ando, M.

M. Maemondo, A. Inoue, K. Kobayashi, S. Sugawara, S. Oizumi, H. Isobe, A. Gemma, M. Harada, H. Yoshizawa, I. Kinoshita, Y. Fujita, S. Okinaga, H. Hirano, K. Yoshimori, T. Harada, T. Ogura, M. Ando, H. Miyazawa, M. S. T. Tanaka, Y. Saijo, K. Hagiwara, S. Morita, and T. Nukiwa, “Geftinib or chemotherapy for non-small-cell lung cancer with mutated EGFR,” N. Engl. J. Med. 362, 2380–2388 (2010).

Andrew, P.

P. Andrew and W. L. Barnes, “Energy transfer across a metal film mediated by surface plasmon polaritons,” Science 306(5698), 1002–1005 (2004).
[Crossref] [PubMed]

Aoe, K.

K. Ohashi, L. V. Sequist, M. E. Arcila, T. Moran, J. Chmielecki, Y. L. Lin, Y. Pan, L. Wang, E. de Stanchina, K. Shien, K. Aoe, S. Toyooka, K. Kiura, L. Fernandez-Cuesta, P. Fidias, J. C. Yang, V. A. Miller, G. J. Riely, M. G. Kris, J. A. Engelman, C. L. Vnencak-Jones, D. Dias-Santagata, M. Ladanyi, and W. Pao, “Lung cancers with acquired resistance to EGFR inhibitors occasionally harbor BRAF gene mutations but lack mutations in KRAS, NRAS, or MEK1,” Proc. Natl. Acad. Sci. U.S.A. 109(31), E2127–E2133 (2012).
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Arcila, M. E.

K. Ohashi, L. V. Sequist, M. E. Arcila, T. Moran, J. Chmielecki, Y. L. Lin, Y. Pan, L. Wang, E. de Stanchina, K. Shien, K. Aoe, S. Toyooka, K. Kiura, L. Fernandez-Cuesta, P. Fidias, J. C. Yang, V. A. Miller, G. J. Riely, M. G. Kris, J. A. Engelman, C. L. Vnencak-Jones, D. Dias-Santagata, M. Ladanyi, and W. Pao, “Lung cancers with acquired resistance to EGFR inhibitors occasionally harbor BRAF gene mutations but lack mutations in KRAS, NRAS, or MEK1,” Proc. Natl. Acad. Sci. U.S.A. 109(31), E2127–E2133 (2012).
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K. Takezawa, V. Pirazzoli, M. E. Arcila, C. A. Nebhan, X. Song, E. de Stanchina, K. Ohashi, Y. Y. Janjigian, P. J. Spitzler, M. A. Melnick, G. J. Riely, M. G. Kris, V. A. Miller, M. Ladanyi, K. Politi, and W. Pao, “HER2 amplification: a potential mechanism of acquired resistance to EGFR inhibition in EGFR-mutant lung cancers that lack the second-site EGFRT790M mutation,” Cancer Discov. 2(10), 922–933 (2012).
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Armour, A. A.

T. S. Mok, Y. L. Wu, S. Thongprasert, C. H. Yang, D. T. Chu, N. Saijo, P. Sunpaweravong, B. Han, B. Margono, Y. Ichinose, Y. Nishiwaki, Y. Ohe, J. J. Yang, B. Chewaskulyong, H. Jiang, E. L. Duffield, C. L. Watkins, A. A. Armour, and M. Fukuoka, “Gefitinib or carboplatin-paclitaxel in pulmonary adenocarcinoma,” N. Engl. J. Med. 361(10), 947–957 (2009).
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Arnold, L.

J. D. Moyer, E. G. Barbacci, K. K. Iwata, L. Arnold, B. Boman, A. Cunningham, C. DiOrio, J. Doty, M. J. Morin, M. P. Moyer, M. Neveu, V. A. Pollack, L. R. Pustilnik, M. M. Reynolds, D. Sloan, A. Theleman, and P. Miller, “Induction of apoptosis and cell cycle arrest by CP-358,774, an inhibitor of epidermal growth factor receptor tyrosine kinase,” Cancer Res. 57(21), 4838–4848 (1997).
[PubMed]

Artal, A.

R. Rosell, E. Carcereny, R. Gervais, A. Vergnenegre, B. Massuti, E. Felip, R. Palmero, R. Garcia-Gomez, C. Pallares, J. M. Sanchez, R. Porta, M. Cobo, P. Garrido, F. Longo, T. Moran, A. Insa, F. De Marinis, R. Corre, I. Bover, A. Illiano, E. Dansin, J. de Castro, M. Milella, N. Reguart, G. Altavilla, U. Jimenez, M. Provencio, M. A. Moreno, J. Terrasa, J. Muñoz-Langa, J. Valdivia, D. Isla, M. Domine, O. Molinier, J. Mazieres, N. Baize, R. Garcia-Campelo, G. Robinet, D. Rodriguez-Abreu, G. Lopez-Vivanco, V. Gebbia, L. Ferrera-Delgado, P. Bombaron, R. Bernabe, A. Bearz, A. Artal, E. Cortesi, C. Rolfo, M. Sanchez-Ronco, A. Drozdowskyj, C. Queralt, I. de Aguirre, J. L. Ramirez, J. J. Sanchez, M. A. Molina, M. Taron, and L. Paz-Ares, “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,” Lancet Oncol. 13(3), 239–246 (2012).
[Crossref] [PubMed]

Asami, K.

T. Mitsudomi, S. Morita, Y. Yatabe, S. Negoro, I. Okamoto, J. Tsurutani, T. Seto, M. Satouchi, H. Tada, T. Hirashima, K. Asami, N. Katakami, M. Takada, H. Yoshioka, K. Shibata, S. Kudoh, E. Shimizu, H. Saito, S. Toyooka, K. Nakagawa, and M. Fukuoka, “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,” Lancet Oncol. 11(2), 121–128 (2010).
[Crossref] [PubMed]

Ashton, S. E.

A. J. Barker, K. H. Gibson, W. Grundy, A. A. Godfrey, J. J. Barlow, M. P. Healy, J. R. Woodburn, S. E. Ashton, B. J. Curry, L. Scarlett, L. Henthorn, and L. Richards, “Studies leading to the identification of ZD1839 (IRESSA): an orally active, selective epidermal growth factor receptor tyrosine kinase inhibitor targeted to the treatment of cancer,” Bioorg. Med. Chem. Lett. 11(14), 1911–1914 (2001).
[Crossref] [PubMed]

Baize, N.

R. Rosell, E. Carcereny, R. Gervais, A. Vergnenegre, B. Massuti, E. Felip, R. Palmero, R. Garcia-Gomez, C. Pallares, J. M. Sanchez, R. Porta, M. Cobo, P. Garrido, F. Longo, T. Moran, A. Insa, F. De Marinis, R. Corre, I. Bover, A. Illiano, E. Dansin, J. de Castro, M. Milella, N. Reguart, G. Altavilla, U. Jimenez, M. Provencio, M. A. Moreno, J. Terrasa, J. Muñoz-Langa, J. Valdivia, D. Isla, M. Domine, O. Molinier, J. Mazieres, N. Baize, R. Garcia-Campelo, G. Robinet, D. Rodriguez-Abreu, G. Lopez-Vivanco, V. Gebbia, L. Ferrera-Delgado, P. Bombaron, R. Bernabe, A. Bearz, A. Artal, E. Cortesi, C. Rolfo, M. Sanchez-Ronco, A. Drozdowskyj, C. Queralt, I. de Aguirre, J. L. Ramirez, J. J. Sanchez, M. A. Molina, M. Taron, and L. Paz-Ares, “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,” Lancet Oncol. 13(3), 239–246 (2012).
[Crossref] [PubMed]

Balak, M.

J. Bean, C. Brennan, J. Y. Shih, G. Riely, A. Viale, L. Wang, D. Chitale, N. Motoi, J. Szoke, S. Broderick, M. Balak, W. C. Chang, C. J. Yu, A. Gazdar, H. Pass, V. Rusch, W. Gerald, S. F. Huang, P. C. Yang, V. Miller, M. Ladanyi, C. H. Yang, and W. Pao, “MET amplification occurs with or without T790M mutations in EGFR mutant lung tumors with acquired resistance to gefitinib or erlotinib,” Proc. Natl. Acad. Sci. U.S.A. 104(52), 20932–20937 (2007).
[Crossref] [PubMed]

Barbacci, E. G.

J. D. Moyer, E. G. Barbacci, K. K. Iwata, L. Arnold, B. Boman, A. Cunningham, C. DiOrio, J. Doty, M. J. Morin, M. P. Moyer, M. Neveu, V. A. Pollack, L. R. Pustilnik, M. M. Reynolds, D. Sloan, A. Theleman, and P. Miller, “Induction of apoptosis and cell cycle arrest by CP-358,774, an inhibitor of epidermal growth factor receptor tyrosine kinase,” Cancer Res. 57(21), 4838–4848 (1997).
[PubMed]

Barker, A. J.

A. J. Barker, K. H. Gibson, W. Grundy, A. A. Godfrey, J. J. Barlow, M. P. Healy, J. R. Woodburn, S. E. Ashton, B. J. Curry, L. Scarlett, L. Henthorn, and L. Richards, “Studies leading to the identification of ZD1839 (IRESSA): an orally active, selective epidermal growth factor receptor tyrosine kinase inhibitor targeted to the treatment of cancer,” Bioorg. Med. Chem. Lett. 11(14), 1911–1914 (2001).
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Barlow, J. J.

A. J. Barker, K. H. Gibson, W. Grundy, A. A. Godfrey, J. J. Barlow, M. P. Healy, J. R. Woodburn, S. E. Ashton, B. J. Curry, L. Scarlett, L. Henthorn, and L. Richards, “Studies leading to the identification of ZD1839 (IRESSA): an orally active, selective epidermal growth factor receptor tyrosine kinase inhibitor targeted to the treatment of cancer,” Bioorg. Med. Chem. Lett. 11(14), 1911–1914 (2001).
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Barnes, W. L.

P. Andrew and W. L. Barnes, “Energy transfer across a metal film mediated by surface plasmon polaritons,” Science 306(5698), 1002–1005 (2004).
[Crossref] [PubMed]

Barrios, C. H.

S. S. Ramalingam, F. Blackhall, M. Krzakowski, C. H. Barrios, K. Park, I. Bover, D. Seog Heo, R. Rosell, D. C. Talbot, R. Frank, S. P. Letrent, A. Ruiz-Garcia, I. Taylor, J. Q. Liang, A. K. Campbell, J. O’Connell, and M. Boyer, “Randomized phase II study of dacomitinib (PF-00299804), an irreversible pan-human epidermal growth factor receptor inhibitor, versus erlotinib in patients with advanced non-small-cell lung cancer,” J. Clin. Oncol. 30(27), 3337–3344 (2012).
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Barthorpe, S.

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R. Rosell, E. Carcereny, R. Gervais, A. Vergnenegre, B. Massuti, E. Felip, R. Palmero, R. Garcia-Gomez, C. Pallares, J. M. Sanchez, R. Porta, M. Cobo, P. Garrido, F. Longo, T. Moran, A. Insa, F. De Marinis, R. Corre, I. Bover, A. Illiano, E. Dansin, J. de Castro, M. Milella, N. Reguart, G. Altavilla, U. Jimenez, M. Provencio, M. A. Moreno, J. Terrasa, J. Muñoz-Langa, J. Valdivia, D. Isla, M. Domine, O. Molinier, J. Mazieres, N. Baize, R. Garcia-Campelo, G. Robinet, D. Rodriguez-Abreu, G. Lopez-Vivanco, V. Gebbia, L. Ferrera-Delgado, P. Bombaron, R. Bernabe, A. Bearz, A. Artal, E. Cortesi, C. Rolfo, M. Sanchez-Ronco, A. Drozdowskyj, C. Queralt, I. de Aguirre, J. L. Ramirez, J. J. Sanchez, M. A. Molina, M. Taron, and L. Paz-Ares, “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,” Lancet Oncol. 13(3), 239–246 (2012).
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S. Kobayashi, T. J. Boggon, T. Dayaram, P. A. Jänne, O. Kocher, M. Meyerson, B. E. Johnson, M. J. Eck, D. G. Tenen, and B. Halmos, “EGFR mutation and resistance of non-small-cell lung cancer to gefitinib,” N. Engl. J. Med. 352(8), 786–792 (2005).
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J. Guillermo Paez, P. Pasi Janne, J. C. Lee, S. Tracy, H. Greulich, S. Gabriel, P. Herman, F. J. Kaye, N. Lindeman, T. J. Boggon, K. Naoki, H. Sasaki, Y. Fujii, M. J. Eck, W. R. Sellers, B. E. Johnson, and M. Meyerson, “EGFR mutations in lung cancer: correlation with clinical response to geftinib therapy,” Science 304, 1497–1500 (2004).
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Kinoshita, I.

M. Maemondo, A. Inoue, K. Kobayashi, S. Sugawara, S. Oizumi, H. Isobe, A. Gemma, M. Harada, H. Yoshizawa, I. Kinoshita, Y. Fujita, S. Okinaga, H. Hirano, K. Yoshimori, T. Harada, T. Ogura, M. Ando, H. Miyazawa, M. S. T. Tanaka, Y. Saijo, K. Hagiwara, S. Morita, and T. Nukiwa, “Geftinib or chemotherapy for non-small-cell lung cancer with mutated EGFR,” N. Engl. J. Med. 362, 2380–2388 (2010).

Kiura, K.

K. Ohashi, L. V. Sequist, M. E. Arcila, T. Moran, J. Chmielecki, Y. L. Lin, Y. Pan, L. Wang, E. de Stanchina, K. Shien, K. Aoe, S. Toyooka, K. Kiura, L. Fernandez-Cuesta, P. Fidias, J. C. Yang, V. A. Miller, G. J. Riely, M. G. Kris, J. A. Engelman, C. L. Vnencak-Jones, D. Dias-Santagata, M. Ladanyi, and W. Pao, “Lung cancers with acquired resistance to EGFR inhibitors occasionally harbor BRAF gene mutations but lack mutations in KRAS, NRAS, or MEK1,” Proc. Natl. Acad. Sci. U.S.A. 109(31), E2127–E2133 (2012).
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Klüter, S.

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Kobayashi, S.

S. Kobayashi, T. J. Boggon, T. Dayaram, P. A. Jänne, O. Kocher, M. Meyerson, B. E. Johnson, M. J. Eck, D. G. Tenen, and B. Halmos, “EGFR mutation and resistance of non-small-cell lung cancer to gefitinib,” N. Engl. J. Med. 352(8), 786–792 (2005).
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Kocher, O.

S. Kobayashi, T. J. Boggon, T. Dayaram, P. A. Jänne, O. Kocher, M. Meyerson, B. E. Johnson, M. J. Eck, D. G. Tenen, and B. Halmos, “EGFR mutation and resistance of non-small-cell lung cancer to gefitinib,” N. Engl. J. Med. 352(8), 786–792 (2005).
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Kogera, F.

M. J. Garnett, E. J. Edelman, S. J. Heidorn, C. D. Greenman, A. Dastur, K. W. Lau, P. Greninger, I. R. Thompson, X. Luo, J. Soares, Q. Liu, F. Iorio, D. Surdez, L. Chen, R. J. Milano, G. R. Bignell, A. T. Tam, H. Davies, J. A. Stevenson, S. Barthorpe, S. R. Lutz, F. Kogera, K. Lawrence, A. McLaren-Douglas, X. Mitropoulos, T. Mironenko, H. Thi, L. Richardson, W. Zhou, F. Jewitt, T. Zhang, P. O’Brien, J. L. Boisvert, S. Price, W. Hur, W. Yang, X. Deng, A. Butler, H. G. Choi, J. W. Chang, J. Baselga, I. Stamenkovic, J. A. Engelman, S. V. Sharma, O. Delattre, J. Saez-Rodriguez, N. S. Gray, J. Settleman, P. A. Futreal, D. A. Haber, M. R. Stratton, S. Ramaswamy, U. McDermott, and C. H. Benes, “Systematic identification of genomic markers of drug sensitivity in cancer cells,” Nature 483(7391), 570–575 (2012).
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Koker, M.

M. L. Sos, H. B. Rode, S. Heynck, M. Peifer, F. Fischer, S. Klüter, V. G. Pawar, C. Reuter, J. M. Heuckmann, J. Weiss, L. Ruddigkeit, M. Rabiller, M. Koker, J. R. Simard, M. Getlik, Y. Yuza, T. H. Chen, H. Greulich, R. K. Thomas, and D. Rauh, “Chemogenomic profiling provides insights into the limited activity of irreversible EGFR Inhibitors in tumor cells expressing the T790M EGFR resistance mutation,” Cancer Res. 70(3), 868–874 (2010).
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J. A. Engelman, K. Zejnullahu, T. Mitsudomi, Y. Song, C. Hyland, J. O. Park, N. Lindeman, C. M. Gale, X. Zhao, J. Christensen, T. Kosaka, A. J. Holmes, A. M. Rogers, F. Cappuzzo, T. Mok, C. Lee, B. E. Johnson, L. C. Cantley, and P. A. Jänne, “MET amplification leads to gefitinib resistance in lung cancer by activating ERBB3 signaling,” Science 316(5827), 1039–1043 (2007).
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Kris, M.

W. Pao, V. Miller, M. Zakowski, J. Doherty, K. Politi, I. Sarkaria, B. Singh, R. Heelan, V. Rusch, L. Fulton, E. Mardis, D. Kupfer, R. Wilson, M. Kris, and H. Varmus, “EGF receptor gene mutations are common in lung cancers from “never smokers” and are associated with sensitivity of tumors to gefitinib and erlotinib,” Proc. Natl. Acad. Sci. U.S.A. 101(36), 13306–13311 (2004).
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Kris, M. G.

K. Takezawa, V. Pirazzoli, M. E. Arcila, C. A. Nebhan, X. Song, E. de Stanchina, K. Ohashi, Y. Y. Janjigian, P. J. Spitzler, M. A. Melnick, G. J. Riely, M. G. Kris, V. A. Miller, M. Ladanyi, K. Politi, and W. Pao, “HER2 amplification: a potential mechanism of acquired resistance to EGFR inhibition in EGFR-mutant lung cancers that lack the second-site EGFRT790M mutation,” Cancer Discov. 2(10), 922–933 (2012).
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K. Ohashi, L. V. Sequist, M. E. Arcila, T. Moran, J. Chmielecki, Y. L. Lin, Y. Pan, L. Wang, E. de Stanchina, K. Shien, K. Aoe, S. Toyooka, K. Kiura, L. Fernandez-Cuesta, P. Fidias, J. C. Yang, V. A. Miller, G. J. Riely, M. G. Kris, J. A. Engelman, C. L. Vnencak-Jones, D. Dias-Santagata, M. Ladanyi, and W. Pao, “Lung cancers with acquired resistance to EGFR inhibitors occasionally harbor BRAF gene mutations but lack mutations in KRAS, NRAS, or MEK1,” Proc. Natl. Acad. Sci. U.S.A. 109(31), E2127–E2133 (2012).
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W. Pao, V. A. Miller, K. A. Politi, G. J. Riely, R. Somwar, M. F. Zakowski, M. G. Kris, and H. Varmus, “Acquired resistance of lung adenocarcinomas to gefitinib or erlotinib is associated with a second mutation in the EGFR kinase domain,” PLoS Med. 2(3), e73 (2005).
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S. S. Ramalingam, F. Blackhall, M. Krzakowski, C. H. Barrios, K. Park, I. Bover, D. Seog Heo, R. Rosell, D. C. Talbot, R. Frank, S. P. Letrent, A. Ruiz-Garcia, I. Taylor, J. Q. Liang, A. K. Campbell, J. O’Connell, and M. Boyer, “Randomized phase II study of dacomitinib (PF-00299804), an irreversible pan-human epidermal growth factor receptor inhibitor, versus erlotinib in patients with advanced non-small-cell lung cancer,” J. Clin. Oncol. 30(27), 3337–3344 (2012).
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Kudoh, S.

T. Mitsudomi, S. Morita, Y. Yatabe, S. Negoro, I. Okamoto, J. Tsurutani, T. Seto, M. Satouchi, H. Tada, T. Hirashima, K. Asami, N. Katakami, M. Takada, H. Yoshioka, K. Shibata, S. Kudoh, E. Shimizu, H. Saito, S. Toyooka, K. Nakagawa, and M. Fukuoka, “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,” Lancet Oncol. 11(2), 121–128 (2010).
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Kupfer, D.

W. Pao, V. Miller, M. Zakowski, J. Doherty, K. Politi, I. Sarkaria, B. Singh, R. Heelan, V. Rusch, L. Fulton, E. Mardis, D. Kupfer, R. Wilson, M. Kris, and H. Varmus, “EGF receptor gene mutations are common in lung cancers from “never smokers” and are associated with sensitivity of tumors to gefitinib and erlotinib,” Proc. Natl. Acad. Sci. U.S.A. 101(36), 13306–13311 (2004).
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Lacouture, M. E.

B. Burtness, M. Anadkat, S. Basti, M. Hughes, M. E. Lacouture, J. S. McClure, P. L. Myskowski, J. Paul, C. S. Perlis, L. Saltz, and S. Spencer, “NCCN Task Force Report: Management of dermatologic and other toxicities associated with EGFR inhibition in patients with cancer,” J. Natl. Compr. Canc. Netw. 7(1), S5–S21, quiz S22–S24 (2009).
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Ladanyi, M.

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R. Rosell, E. Carcereny, R. Gervais, A. Vergnenegre, B. Massuti, E. Felip, R. Palmero, R. Garcia-Gomez, C. Pallares, J. M. Sanchez, R. Porta, M. Cobo, P. Garrido, F. Longo, T. Moran, A. Insa, F. De Marinis, R. Corre, I. Bover, A. Illiano, E. Dansin, J. de Castro, M. Milella, N. Reguart, G. Altavilla, U. Jimenez, M. Provencio, M. A. Moreno, J. Terrasa, J. Muñoz-Langa, J. Valdivia, D. Isla, M. Domine, O. Molinier, J. Mazieres, N. Baize, R. Garcia-Campelo, G. Robinet, D. Rodriguez-Abreu, G. Lopez-Vivanco, V. Gebbia, L. Ferrera-Delgado, P. Bombaron, R. Bernabe, A. Bearz, A. Artal, E. Cortesi, C. Rolfo, M. Sanchez-Ronco, A. Drozdowskyj, C. Queralt, I. de Aguirre, J. L. Ramirez, J. J. Sanchez, M. A. Molina, M. Taron, and L. Paz-Ares, “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,” Lancet Oncol. 13(3), 239–246 (2012).
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M. J. Garnett, E. J. Edelman, S. J. Heidorn, C. D. Greenman, A. Dastur, K. W. Lau, P. Greninger, I. R. Thompson, X. Luo, J. Soares, Q. Liu, F. Iorio, D. Surdez, L. Chen, R. J. Milano, G. R. Bignell, A. T. Tam, H. Davies, J. A. Stevenson, S. Barthorpe, S. R. Lutz, F. Kogera, K. Lawrence, A. McLaren-Douglas, X. Mitropoulos, T. Mironenko, H. Thi, L. Richardson, W. Zhou, F. Jewitt, T. Zhang, P. O’Brien, J. L. Boisvert, S. Price, W. Hur, W. Yang, X. Deng, A. Butler, H. G. Choi, J. W. Chang, J. Baselga, I. Stamenkovic, J. A. Engelman, S. V. Sharma, O. Delattre, J. Saez-Rodriguez, N. S. Gray, J. Settleman, P. A. Futreal, D. A. Haber, M. R. Stratton, S. Ramaswamy, U. McDermott, and C. H. Benes, “Systematic identification of genomic markers of drug sensitivity in cancer cells,” Nature 483(7391), 570–575 (2012).
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Reynolds, M. M.

J. D. Moyer, E. G. Barbacci, K. K. Iwata, L. Arnold, B. Boman, A. Cunningham, C. DiOrio, J. Doty, M. J. Morin, M. P. Moyer, M. Neveu, V. A. Pollack, L. R. Pustilnik, M. M. Reynolds, D. Sloan, A. Theleman, and P. Miller, “Induction of apoptosis and cell cycle arrest by CP-358,774, an inhibitor of epidermal growth factor receptor tyrosine kinase,” Cancer Res. 57(21), 4838–4848 (1997).
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J. Bean, C. Brennan, J. Y. Shih, G. Riely, A. Viale, L. Wang, D. Chitale, N. Motoi, J. Szoke, S. Broderick, M. Balak, W. C. Chang, C. J. Yu, A. Gazdar, H. Pass, V. Rusch, W. Gerald, S. F. Huang, P. C. Yang, V. Miller, M. Ladanyi, C. H. Yang, and W. Pao, “MET amplification occurs with or without T790M mutations in EGFR mutant lung tumors with acquired resistance to gefitinib or erlotinib,” Proc. Natl. Acad. Sci. U.S.A. 104(52), 20932–20937 (2007).
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K. Takezawa, V. Pirazzoli, M. E. Arcila, C. A. Nebhan, X. Song, E. de Stanchina, K. Ohashi, Y. Y. Janjigian, P. J. Spitzler, M. A. Melnick, G. J. Riely, M. G. Kris, V. A. Miller, M. Ladanyi, K. Politi, and W. Pao, “HER2 amplification: a potential mechanism of acquired resistance to EGFR inhibition in EGFR-mutant lung cancers that lack the second-site EGFRT790M mutation,” Cancer Discov. 2(10), 922–933 (2012).
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Figures (7)

Fig. 1
Fig. 1 Experimental system and optofluidic resonator. (a) Experimental setup. (b) optofluidic resonator; five layers from top to bottom: A 0.3-mm thick glass slide with 35 nm sliver on top, 10 × 4 mm2 rectangle channel embedded in a 0.5-mm-thick glass slab working as sample container in the guiding layer, and another 0.3-mm-thick glass coated with 300-nm-thick sliver at the bottom of the structure, the middle three layers form the guiding layer of the waveguide. These parts are optically contacted together and parallel to each other. Light is coupled into the sample channel of the fluidic resonator. (c) AZD9291, gefitinib and erlotinib drug molecular structures and NSCLC-EGFR molecular structure [37]. (d) reflectivity of light R and coupled angle θ changed, when the refraction index of the sample changed. The refractive index of the sample changed Δn=2.0× 10 5 and the ATR position shifted, such that the ATR dip would shift.
Fig. 2
Fig. 2 EGFR protein and patient serum has same effect to promote the cancer cell growth and multiplication. (a) and (b) NSCLC biopsies from a terminal cancer patient at Zhejiang Rongjun Hospital. Small tissue samples can be obtained and examined under the microscope to confirm the diagnosis. (c) As a comparison task, to estimated the NSCLC patient serum and NSCLC EGFR protein have same effect to promote the proliferation of cancer cell. (d) At t = 0h, the picture has present that the same amount of NSCLC cell 10μL has been injected into culture tube 1-4. (e) After 24 hours, 1-4 culture tube has different cell amount. In the 4 and 2 culture tube, the amount of NSCLC cell has 80μL and 100μL, respectively. However, the amount of NSCLC cell keeps 10μL in the 1 and 3 culture tube.
Fig. 3
Fig. 3 Drugs, NSCLC cell, and the refraction index of the sample changed in an optofluidic resonator. (a-d) NSCLC cell has been cultured in different drug culture tube, as shown in Table 1. And we have to measure culture tube RI every 6 hours to observation of cell growth and multiplication. (e) After 24 hours, the 1-4 culture tube has different amount of NSCLC cell. (f) NSCLC cell be obtained and examined under the microscope to confirm the diagnosis from culture tube. (g) The amount of NSCLC cell has been measured every 6 hours for every culture tube.
Fig. 4
Fig. 4 Drugs, NSCLC-EGFR molecules, and the refraction index of the sample changed in an optofluidic resonator. (a-c) ATR spectrum for different times when drugs were injected into the resonator. c-d present AZD9291, erlotinib and gefitinib, respectively. (d) Different drug ATR dip images.
Fig. 5
Fig. 5 Monitoring of interaction times by ATR dip shift. (a) AZD9291 interactions with NSCLC-EGFR molecules to find the interaction time from 0 s to 12 s; after 12 s the ATR dip e shift stopped. (b) Gefitinib interaction with NSCLC-EGFR molecule; ATR dip shift does not change significantly from 0 s to 14 s, but there is a significant, continuous change after 14 s and the united ATR dip shift remains stopped after 24 s. (c) Erlotinib interactions with NSCLC-EGFR molecules; the ATR dip shift maintains the same position for the entire duration. (d-f) calculation of one ATR dip shift in experimental images by MATLAB R2014a, showing AZD9291, gefitinib and erlotinib interacting with a NSCLC-EGFR molecule. (g) the ATR dip shift changed from 0 s to 24 s, including AZD9291, gefitinib and erlotinib.
Fig. 6
Fig. 6 Label-free analysis of efficiency by fluorescence. (a) Three ATR dip in the experimental image. In the centre, we removed a black area 1.0 mm*1.0 mm. (b) the black area was magnified twenty times using a microscopic system and red and blue faculae in the image. (c) Quantity, size and intensity of red and blue faculae remain unchanged after removing the background gradient to show the obvious fluorescence. (d,f) Red facula is the NSCLC-EGFR molecule fluorescence and spectra at before drug is injected hollow-core. (e,g) blue faculae is the drug fluorescence and spectra before NSCLC-EGFR molecule solution is injected hollow-core. (h-j) the proportion measurement of NSCLC-EGFR fluorescence spot area in a 2 mm*2 mm area at 0 s, 5 s, 10 s and 20 s.
Fig. 7
Fig. 7 Calculation and comparison of fluorescence intensity for NSCLC-EGFR molecular interaction with AZD9291, gefitinib and erlotinib. (a) We removed a black area 1 mm*1 mm and calculated the fluorescence faculae area hold proportion in the 1 mm2. When the NSCLC-EGFR molecule solution was injected into the cavity, the occupation ratio of red fluorescence faculae was 0.3039. Occupation ratios of 0.0924, 0.1811 and 0.2305 were seen for AZD9291, gefitinib and erlotinib after 28 s when injected into the cavity, respectively. The occupation ratios of blue fluorescence faculae are 0.0333, 0.0266 and 0.0236. (b-d) AZD9291, gefitinib, erlotinib and the NSCLC-EGFR molecule are the same size, and the solution concentration was 1.0 μg/ml. (e) EGFR molecule content reduction and total drug dosage.

Tables (1)

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Table 1 NSCLC cell has been cultured in different drug culture tube

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