Rebiopsy in IV stage non-small-cell lung cancer patients after systemic therapy


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Abstract

Rebiopsies are not performed in currently clinical practice for the patients with advanced non-small cell lung cancer (NSCLC). However, identification of as an activating mutation, as other molecular and genetic disorders can considerably change management and prognosis for these patients. Twenty-nine patients with advanced NSCLC after systemic therapy were rebiopsied and samples were studied for a limited range of genetic alterations (sensitizing EGFR mutations, T790M, KRAS gene mutations, translocation of ALK, ROS1, expression PD-L1). Results were used for making decision on further treatment.

About the authors

Denis I. Yudin

N.N. Blokhin Russian Cancer Research Center

Email: yudinden@mail.ru
MD, PhD; Senior researcher of the Department of clinical biotechnology Moscow, 115478, Russian Federation

A. A Anteev

N.N. Blokhin Russian Cancer Research Center

Moscow, 115478, Russian Federation

D. T Marinov

N.N. Blokhin Russian Cancer Research Center

Moscow, 115478, Russian Federation

M. S Ardzinba

N.N. Blokhin Russian Cancer Research Center

Moscow, 115478, Russian Federation

K. K Laktionov

N.N. Blokhin Russian Cancer Research Center

Moscow, 115478, Russian Federation

References

  1. Давыдов М.И., Аксель Е.М. Статистика злокачественных новообразований в России и странах СНГ в 2009. Вестник РОНЦ им. Н.Н. Блохина РАМН. 2011: 22 (3, прил. 1).
  2. Зборовская И.Б. Современные стратегии исследования маркеров опухолевого роста в клинической практике. Успехи молекулярной онкологии. 2014; 1 (2): 4-15.
  3. Аллахвердиев А.К., Лактионов К.К., Полоцкий Б.Е., Давыдов М.И. Современные возможности видеоторакоскопии в практике торакальной онкологии. Вестник Московского онкологического общества. 2009; (6-8).
  4. Johnson B.E., Kris M.G., Berry L.D. et al. A multicenter effort to identify driver mutations and employ targeted therapy in patients with lung adenocarcinomas: The Lung Cancer Mutation Consortium (LCMC). J. Clin. Oncol. 2013; 31 (Suppl.): Abstr. 8019.
  5. Mok T.S., Wu Y.L., Thongprasert S. et al. Gefitinib or carboplatin-paclitaxel in pulmonary adenocarcinoma. N. Engl. J. Med. 2009; 361: 947-57.
  6. Maemondo M., Inoue A., Kobayashi K. et al. North-East Japan Study Group. Gefitinib or chemotherapy for non-small-cell lung cancer with mutated EGFR. N. Engl. J. Med. 2010; 362: 2380-8.
  7. Zhou C., Wu Y.L., Chen G. et al. Erlotinib versus chemotherapy as first-line treatment for patients with advanced EGFR mutation-positive non-small-cell lung cancer (OPTIMAL, CTONG-0802): a multicentre, openlabel, randomised, phase 3 study. Lancet Oncol. 2011; 12: 735-42.
  8. Rosell R., Carcereny E., Gervais R. et al. Spanish Lung Cancer Group in collaboration with Groupe Français de Pneumo-Cancérologie and Associazione Italiana Oncologia Toracica. 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. 2012; 13: 239-46.
  9. Fiala O., Pesek M., Finek J., Krejci J., Bortlicek Z., Benesova L., Minarik M. Second line treatment in advanced non-small cell lung cancer (NSCLC): comparison of efficacy of erlotinib and chemotherapy. Neoplasma. 2013; 60 (2): 129-34.
  10. NCCN guidelines, ver. 1.2014. www.nccn.org
  11. Sequist L.V., Waltman B.A., Dias-Santagata D. et al. Genotypic and histological evolution of lung cancers acquiring resistance to EGFR inhibitors. Sci. Transl. Med. 2011; 3: 75ra26.
  12. Ohashi K., Sequist L.V., Arcila M.E. et al. 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. 2012; 109: E2127-33.
  13. Kwak E.L., Bang Y.J., Camidge D.R. et al. Anaplastic lymphoma kinase inhibition in non-small-cell lung cancer.et al. N. Engl. J. Med. 2010; 363 (18): 1693-703.
  14. Garber K. ALK, lung cancer, and personalized therapy: portent of the future. J. Natl. Cancer Inst. 2010; 102 (10): 672-5. doi: 10.1093/jnci/djq184.
  15. Rodig S., Shaw A.T., Costa D. et al., Unique clinicopathologic features characterize ALK-rearranged lung adenocarcinoma in the western population. Clin. Cancer Res. 2009; 15: 5216-23.
  16. Shaw A., Costa D., Mino-Kenudson M. et al. Clinical features and outcome of patients with non-small-cell lung cancer who harbor EML4-ALK. J. Clin. Oncol. 2009; 27: 4247-53.
  17. Zhang X., Zhang Sh., Yang X., Yang J., Zhou Q., Yin L. et al. Fusion of EML4 and ALK is associated with development of lung adenocarcinomas lacking EGFR and KRAS mutations and is correlated with ALK expression. Mol. Cancer. 2010; 9: Article 188.
  18. Tan W., Wilner K.D., Bang Y., Kwak E.L., Maki R.G., Camidge D.R. et al. Pharmacokinetics (PK) of PF-02341066, a dual ALK/MET inhibitor after multiple oral doses to advanced cancer patients. J. Clin. Oncol. 2010; 28 (15S): Abstr. 2596.
  19. Camidge D.R., Bang Y., Kwak E.L. et al. Progression-free survival from a phase I study of crizotinib (PF-02341066) in patients with ALK-positive non-small cell lung cancer. J. Clin. Oncol. 2011; 29 (Suppl.): Abstr. 2501.
  20. Shaw A.T., Kim D-W, Nakagawa K. et al. Crizotinib versus chemotherapy in advanced ALK-positive lung cancer. N. Engl. J. Med. 2013; 368 (25): 2385-94. doi: 10.1056/NEJMoa1214886.
  21. Katayama R., Shaw A.T., Khan T.M. et al. Mechanisms of acquired crizotinib resistance in ALK-rearranged lung cancers. Sci. Transl. Med. 2012; 4 (120): 120ra17.
  22. Shaw A.T., Kim D.W., Mehra R., Tan D.S., Felip E., Chow L.Q. et al. Ceritinib in ALK-rearranged non-small-cell lung cancer. N. Engl. J. Med. 2014; 370: 1189-97.
  23. Zhang S., Wang F., Keats J. et al. Crizotinib-resistant mutants of EML4-ALK identified through an accelerated mutagenesis screen. Chem. Biol. Drug Des. 2011; 78 (6): 999-1005.
  24. Heuckmann J.M., Hölzel M., Sos M.L. et al. ALK mutations conferring differential resistance to structurally diverse ALK inhibitors. Clin. Cancer Res. 2011; 17 (23): 7394-401.
  25. Поляков И.С., Имянитов Е.Н. Молекулярная патология рака легкого: клинические аспекты. Сибирский онкологический журнал. 2013; 60 (6): 48-55.
  26. Jänne P.A., Shaw A.T., Pereira J.R. et al. Selumetinib plus docetaxel for KRAS-mutant advanced non-small-cell lung cancer: a randomised, multicentre, placebo-controlled, phase 2 study. Lancet Oncol. 2013; 14: 38-47.
  27. Borghaei H., Paz-Ares L., Horn L., Spigel D. R. et al. Nivolumab versus docetaxel in advanced nonsquamous non-small-cell lung cancer. N. Engl. J. Med. 2015; 373: 1627-39.
  28. Paz-Ares L., Horn L., Borghaei H., Spigel D.R. et al Phase III, randomized trial (CheckMate 057) of nivolumab (NIVO) versus docetaxel (DOC) in advanced non-squamous cell (non-SQ) non-small cell lung cancer (NSCLC). J. Clin. Oncol. 2015; 33 (Suppl.): Abstr. LBA109.
  29. Herbst R.S., Baas P., Kim D.W., Felip E. et al. Pembrolizumab versus docetaxel for previously treated, PD-L1-positive, advanced non-small-cell lung cancer (KEYNOTE-010): a randomised controlled trial. Lancet. doi: 10.1016/S0140-6736(15)01281-7.

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