Rebiopsy for patients with non-small-cell lung cancer after epidermal growth factor receptor-tyrosine kinase inhibitor failure

Takahisa Kawamura, Hirotsugu Kenmotsu, Tetsuhiko Taira, Shota Omori, Kazuhisa Nakashima, Kazushige Wakuda, Akira Ono, Tateaki Naito, Haruyasu Murakami, Keita Mori, Takashi Nakajima, Yasuhisa Ohde, Masahiro Endo, Toshiaki Takahashi, Takahisa Kawamura, Hirotsugu Kenmotsu, Tetsuhiko Taira, Shota Omori, Kazuhisa Nakashima, Kazushige Wakuda, Akira Ono, Tateaki Naito, Haruyasu Murakami, Keita Mori, Takashi Nakajima, Yasuhisa Ohde, Masahiro Endo, Toshiaki Takahashi

Abstract

Although third-generation epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKI) can overcome T790M-mediated resistance in non-small-cell lung cancer (NSCLC), rebiopsy to confirm T790M status is occasionally difficult. We aimed to investigate the current tendency and the limitations of rebiopsy in clinical practice. This study included 139 consecutive NSCLC patients with EGFR mutations, who had experienced progressive disease (PD) after EGFR-TKI treatment. We retrospectively reviewed patient characteristics, tumor progression sites and rebiopsy procedures. Of 120 patients (out of the original 139) who were eligible for clinical trials, 75 (63%) underwent rebiopsy for 30 pleural effusions, 32 thoracic lesions, four bone, two liver, and seven at other sites. Rebiopsy procedures included 30 thoracocentesis, 24 transbronchial biopsies, 13 computed tomography (CT)-guided needle biopsies and 8 other procedures. Of the 75 rebiopsied patients, 71 (95%) were pathologically diagnosed with malignancy; and 34 (45%) had available tissue samples for EGFR analyses. Of the 75 biopsied patients, 61 (81%) were analyzed for EGFR mutation, using tissue or cytology samples; T790M mutations were identified in 20 (33%) of the 61 patients. Of the 120 patients, 45 (38%) did not undergo rebiopsy, because of inaccessible tumor sites (n = 19), patient refusal (n = 6) or decision of physician (n = 10). In conclusion, among patients with EGFR mutations who had PD after EGFR-TKI treatment, 63% underwent rebiopsy. Most rebiopsy samples were diagnosed with malignancy. However, tissue samples were less available and T790M mutations were identified less frequently than in previous studies. Skill and experience with rebiopsy and noninvasive alternative methods will be increasingly important.

Keywords: Disease progression; T790M mutation; epidermal growth factor receptor-tyrosine kinase inhibitors; non-small-cell lung cancer; rebiopsy.

© 2016 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.

Figures

Figure 1
Figure 1
Overview of rebiopsies among patients with non‐small‐cell lung cancer (NSCLC) treated with early‐version epidermal growth factor receptor‐tyrosine kinase inhibitors (EGFR‐TKI). Patients were tested with the aim of enrolling them in trials for third‐generation EGFR‐TKI, which is notably effective against NSCLC with T790M mutations in the EGFR gene. EGFRMut+, EGFR mutation carrier; PD, progressive disease; PS, performance status.

References

    1. Mok TS, Wu YL, Thongprasert S et al Gefitinib or carboplatin‐paclitaxel in pulmonary adenocarcinoma. N Engl J Med 2009; 361: 947–57.
    1. Maemondo M, Inoue A, Kobayashi K et al Gefitinib or chemotherapy for non‐small‐cell lung cancer with mutated EGFR . N Engl J Med 2010; 362: 2380–8.
    1. Sun JM, Rampal S, Lee G et al Real world impact of epidermal growth factor receptor mutation status on treatment patterns in patients with non‐small‐cell lung cancer. Lung Cancer 2013; 80: 191–6.
    1. Kobayashi S, Boggon TJ, Dayaram T et al EGFR mutation and resistance of non‐small‐cell lung cancer to gefitinib. N Engl J Med 2005; 352: 786–92.
    1. Pao W, Miller VA, Politi KA et al Acquired resistance of lung adenocarcinomas to gefitinib or erlotinib is associated with a second mutation in the EGFR kinase domain. PLoS Med 2005; 2: e73.
    1. Yano S, Yamada T, Takeuchi S et al Hepatocyte growth factor expression in EGFR mutant lung cancer with intrinsic and acquired resistance to tyrosine kinase inhibitors in a Japanese cohort. J Thorac Oncol 2011; 6: 2011–17.
    1. Jänne PA, Yang JC, Kim DW et al AZD9291 in EGFR inhibitor‐resistant non‐small‐cell lung cancer. N Engl J Med 2015; 372: 1689–99.
    1. Sequist LV, Soria JC, Goldman JW et al Rociletinib in EGFR‐mutated non‐small‐cell lung cancer. N Engl J Med 2015; 372: 1700–9.
    1. Goto K, Satouchi M, Ishii G et al An evaluation study of EGFR mutation tests utilized for non‐small‐cell lung cancer in the diagnostic setting. Ann Oncol 2012; 23: 2914–19.
    1. Steuer CE, Khuri FR, Ramalingam SS. The next generation of epidermal growth factor receptor tyrosine kinase inhibitors in the treatment of lung cancer. Cancer 2015; 121: E1–6.
    1. Cross DA, Ashton SE, Ghiorghiu S et al AZD9291, an irreversible EGFR TKI, overcomes T790M‐mediated resistance to EGFR inhibitors in lung cancer. Cancer Discov 2014; 4: 1046–61.
    1. Chouaid C, Dujon C, Do P et al Feasibility and clinical impact of re‐biopsy in advanced non‐small‐cell lung cancer: a prospective multicenter study in a real‐world setting (GFPC study 12‐01). Lung Cancer 2014; 86: 170–3.
    1. Arcila ME, Oxnard GR, Nafa K et al Rebiopsy of lung cancer patients with acquired resistance to EGFR inhibitors and enhanced detection of the T790M mutation using a locked nucleic acid–based assay. Clin Cancer Res 2011; 17: 1169–80.
    1. Yoon HJ, Lee HY, Lee KS et al Repeat biopsy for mutational analysis of non‐small‐cell lung cancers resistant to previous chemotherapy: adequacy and complications. Radiology 2012; 265: 939–48.
    1. Yu HA, Arcila ME, Rekhtman N et al Analysis of tumor specimens at the time of acquired resistance to EGFR‐TKI therapy in 155 patients with EGFR‐mutant lung cancers. Clin Cancer Res 2013; 19: 2240–7.
    1. Hata A, Katakami N, Yoshioka H et al Rebiopsy of non‐small‐cell lung cancer patients with acquired resistance to epidermal growth factor receptor‐tyrosine kinase inhibitor: comparison between T790M mutation‐positive and mutation‐negative populations. Cancer 2013; 119: 4325–32.
    1. Su KY, Chen HY, Li KC et al Pretreatment epidermal growth factor receptor (EGFR) T790M mutation predicts shorter EGFR tyrosine kinase inhibitor response duration in patients with non‐small‐cell lung cancer. J Clin Oncol 2012; 30: 433–40.
    1. Kuiper JL, Heideman DA, Thunnissen E et al Incidence of T790M mutation in (sequential) rebiopsies in EGFR‐mutated NSCLC‐patients. Lung Cancer 2014; 85: 19–24.
    1. Diaz LA Jr, Bardelli A. Liquid biopsies: genotyping circulating tumor DNA. J Clin Oncol 2014; 32: 579–86.
    1. Karlovich C, Goldman JW, Sun JM et al Assessment of EGFR mutation status in matched plasma and tumor tissue of NSCLC patients from a phase I study of rociletinib (CO‐1686). Clin Cancer Res 2016; 22: 2386–95.
    1. Thress KS, Brant R, Carr TH et al EGFR mutation detection in ctDNA from NSCLC patient plasma: a cross‐platform comparison of leading technologies to support the clinical development of AZD9291. Lung Cancer 2015; 90: 509–15.
    1. Jackman D, Pao W, Riely GJ et al Clinical definition of acquired resistance to epidermal growth factor receptor tyrosine kinase inhibitors in non‐small‐cell lung cancer. J Clin Oncol 2010; 28: 357–60.
    1. Sequist LV, Waltman BA, Dias‐Santagata D et al Genotypic and histological evolution of lung cancers acquiring resistance to EGFR inhibitors. Sci Transl Med 2011; 3: 75ra26.
    1. Hata A, Katakami N, Yoshioka H et al Spatiotemporal T790M heterogeneity in individual patients with EGFR‐mutant non‐small‐cell lung cancer after acquired resistance to EGFR‐TKI. J Thorac Oncol 2015; 10: 1553–9.

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