Anaplastic lymphoma kinase as a new target for the treatment of non-small-cell lung cancer

References

• Lynch TJ, Bell DW, Sordella R et al. Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib. N. Engl. J. Med.350, 2129–2139 (2004).
   PubMed Web of Science ®Google Scholar
• Paez JG, Janne PA, Lee JC et al.EGFR mutations in lung cancer: correlation with clinical response to gefitinib therapy. Science304, 1497–1500 (2004).
   PubMed Web of Science ®Google Scholar
• Sequist LV, Bell DW, Lynch TJ et al. Molecular predictors of response to epidermal growth factor receptor antagonists in non-small-cell lung cancer. J. Clin. Oncol.25, 587–595 (2007).
   PubMed Web of Science ®Google Scholar
• Soda M, Choi YL, Enomoto M et al. Identification of the transforming EML4–ALK fusion gene in non-small-cell lung cancer. Nature448, 561–566 (2007).
   PubMed Web of Science ®Google Scholar
• Pulford K, Lamant L, Morris SW et al. Detection of anaplastic lymphoma kinase (ALK) and nucleolar protein nucleophosmin (NPM)-ALK proteins in normal and neoplastic cells with the monoclonal antibody ALK1. Blood89, 1394–1404 (1997).
   PubMed Web of Science ®Google Scholar
• Mosse YP, Wood A, Maris JM. Inhibition of ALK signaling for cancer therapy. Clin. Cancer Res.15, 5609–5614 (2009).
   PubMed Web of Science ®Google Scholar
• Morris SW, Kirstein MN, Valentine MB et al. Fusion of a kinase gene, ALK, to a nucleolar protein gene, NPM, in non-Hodgkin’s lymphoma. Science263, 1281–1284 (1994).
   PubMed Web of Science ®Google Scholar
• Laurent C, Do C, Gascoyne RD et al. Anaplastic lymphoma kinase-positive diffuse large B-cell lymphoma: a rare clinicopathologic entity with poor prognosis. J. Clin. Oncol.27, 4211–4216 (2009).
   PubMed Web of Science ®Google Scholar
• Griffin CA, Hawkins AL, Dvorak C et al. Recurrent involvement of 2p23 in inflammatory myofibroblastic tumors. Cancer Res.59, 2776–2780 (1999).
   PubMed Web of Science ®Google Scholar
• Chen Y, Takita J, Choi YL et al. Oncogenic mutations of ALK kinase in neuroblastoma. Nature455, 971–974 (2008).
   PubMed Web of Science ®Google Scholar
• Takezawa K, Okamoto I, Nishio K et al. Role of ERK-BIM and STAT3-survivin in signaling pathways in ALK inhibitor-induced apoptosis in EML4–ALK-positive lung cancer. Clin. Cancer Res.17, 2140–2148 (2011).
   PubMed Web of Science ®Google Scholar
• Soda M, Takada S, Takeuchi K et al. A mouse model for EML4–ALK-positive lung cancer. Proc. Natl Acad. Sci. USA105, 19893–19897 (2008).
   PubMed Web of Science ®Google Scholar
• Rikova K, Guo A, Zeng Q et al. Global survey of phosphotyrosine signaling identifies oncogenic kinases in lung cancer. Cell131, 1190–203 (2007).
   PubMed Web of Science ®Google Scholar
• Choi YL, Takeuchi K, Soda M et al. Identification of novel isoforms of the EML4–ALK transforming gene in non-small cell lung cancer. Cancer Res.68, 4971–4976 (2008).
   PubMed Web of Science ®Google Scholar
• Sanders HR, Li HR, Bruey JM et al. Exon scanning by reverse transcriptase-polymerase chain reaction for detection of known and novel EML4–ALK fusion variants in non-small cell lung cancer. Cancer Genetics204, 45–42 (2011).
   Google Scholar
• Takeuchi K, Choi YL, Togashi Y et al. KIF5B-ALK, a novel fusion oncokinase identified by an immunohistochemistry-based diagnostic system for ALK-positive lung cancer. Clin. Cancer Res.15(9), 3143–3149 (2009).
   PubMed Web of Science ®Google Scholar
• Wong DW, Leung EL, Wong SK et al. A novel KIF5B-ALK variant in non-small cell lung cancer. Cancer117(12), 2709–2718 (2011).
   PubMed Web of Science ®Google Scholar
• Wong DW, Leung EL, So KK et al. The EML4–ALK fusion gene is involved in various histologic types of lung cancers from nonsmokers with wild-type EGFR and KRAS. Cancer115, 1723–1733 (2009).
   PubMed Web of Science ®Google Scholar
• Rodig SJ, Mino-Kenudson M, Dacic S et al. Unique clinicopathologic features characterize ALK-rearranged lung adenocarcinoma in the western population. Clin. Cancer Res.15, 5216–5223 (2009).
   PubMed Web of Science ®Google Scholar
• Shaw AT, Yeap BY, Mino-Kenudson M et al. Clinical features and outcome of patients with non-small-cell lung cancer who harbour EML4–ALK. J. Clin. Oncol.27, 4247–4253 (2009).
   PubMed Web of Science ®Google Scholar
• Inamura K, Takeuchi K, Togashi Y et al.EML4–ALK lung cancers are characterized by rare other mutations, a TTF-1 cell lineage, an acinar histology, and young onset. Mod. Pathol.22(4), 508–515 (2009).
   PubMed Web of Science ®Google Scholar
• Koh Y, Kim DW, Kim TM et al. Clinicopathologic characteristics and outcome of patients with anaplastic lymphoma kinase-positive advanced pulmonary adenocarcinoma. Suggestion for an effective screening strategy for these tumors. J. Thorac. Oncol.6(5), 905–912 (2011).
   Google Scholar
• Zhang X, Zhang S, Yang X 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. Cancer9, 188 (2010).
   PubMed Web of Science ®Google Scholar
• Sakairi Y, Nakajima T, Yasufuku K et al.EML4–ALK fusion gene assessment using metastatic lymphnode samples obtained by endobronchial ultrasound-guided transbronchiale needle aspiration. Clin. Cancer Res.16, 4938–4945 (2010).
   PubMed Web of Science ®Google Scholar
• Yoshida A, Tsuta K, Watanabe SI et al. Frequent ALK rearrangement and TTF-1/p63 co-expression in lung adenocarcinoma with signet-ring cell component. Lung Cancer.72(3), 309–315 (2011).
   PubMed Web of Science ®Google Scholar
• Koivunen JP, Mermel C, Zejnullahu K et al.EML4–ALK fusion gene and efficacy of an ALK kinase inhibitor in lung cancer. Clin. Cancer Res.14(13), 4275–4283 (2008).
   PubMed Web of Science ®Google Scholar
• Martelli MP, Sozzi G, Hernandez L et al.EML4–ALK rearrangement in non-small cell lung cancer and non-tumor lung tissues. Am. J. Pathol.174, 661–670 (2009).
   PubMed Web of Science ®Google Scholar
• Shinmura K, Kageyama S, Tao H et al.EML4–ALK fusion transcripts, but no NPM- TPM3-, CLTC-, ATIC-, or TFG-ALK fusion transcripts, in non-small cell lung carcinomas. Lung Cancer61, 163–169 (2008).
   PubMed Web of Science ®Google Scholar
• Inamura K, Takeuchi K, Togashi Y et al.EML4–ALK fusion is linked to histological characteristics in a subset of lung cancers. J. Thorac. Oncol.3, 13–17 (2008).
   PubMed Web of Science ®Google Scholar
• Camidge DR, Kono SA, Lu X et al. Anaplastic lymphoma kinase gene rearrangements in non-small cell lung cancer are associated with prolonged progression-free survival on pemetrexed. J. Thorac. Oncol.6, 774–780 (2011).
   PubMed Web of Science ®Google Scholar
• Paik JH, Choe G, Kim H et al. Screening of anaplastic lymphoma kinase rearrangement by immunohistochemistry in non-small cell lung cancer. Correlation with fluorescence in situ hybridization. J. Thorac. Oncol.6(3), 466–472 (2011).
   PubMed Web of Science ®Google Scholar
• Takahashi T, Sonobe M, Kobayashi M et al. Clinicopathologic features of non-small-cell lung cancer with EML4–ALK fusion gene. Ann. Sur. Oncol.17, 889–897 (2009).
   Google Scholar
• Kwak EL, Bang YJ, Camidge DR et al. Anaplastic lymphoma kinase inhibition in non-small-cell lung cancer. N. Engl. J. Med.363(18), 1693–1703 (2010).
   PubMed Web of Science ®Google Scholar
• Boland JM, Erdogan S, Vasmatzis G et al. Anaplastic lymphoma kinase immunoreactivity correlates with ALK gene rearrangement and transcriptional up-regulation in non-small cell lung carcinomas. Hum. Pathol.40, 1152–1158 (2009).
   PubMed Web of Science ®Google Scholar
• Salido M, Pijuan L, Martinez-Aviles L et al. Increased ALK gene copy number and amplification are frequent in non-small cell lung cancer. J. Thorac. Oncol.6(1), 21–27 (2011).
   PubMed Web of Science ®Google Scholar
• Camidge DR, Kono SA, Flacco A et al. Optimizing the detection of lung cancer patients harboring anaplastic lymphoma kinase (ALK) gene rearrangements potentially suitable for ALK inhibitor treatment. Clin. Cancer Res.16(22), 5581–5590 (2010).
   PubMed Web of Science ®Google Scholar
• Sun Y, Ren Y, Fang Z et al. Lung adenocarcinoma from East Asian never-smokers is a disease largely defined by targetable oncogenic mutant kinases. J. Clin. Oncol.28, 4616–4620 (2010).
   PubMed Web of Science ®Google Scholar
• Yi ES, Boland JM, Maleszewski JJ et al. Correlation of IHC and FISH for ALK gene rearrangement in non-small cell lung carcinoma. IHC score algorithm for FISH. J. Thorac. Oncol.6, 459–465 (2011).
   PubMed Web of Science ®Google Scholar
• Shaw AT, Yeap BY, Costa DB et al. prognostic value of ALK rearrangement in metastatic NSCLC. Presented at: American Society of Clinical Oncology Meeting. Chicago, IL, USA, 4–8 June 2010.
   Google Scholar
• Mino-Kenudson M, Chirieac LR, Law K et al. A novel, highly sensitive antibody allows for the routine detection of ALK-rearranged lung adenocarcinomas by standard immunohistochemistry. Clin. Cancer Res.16, 1561–1571 (2010).
   PubMed Web of Science ®Google Scholar
• Tiseo M, Gelsomino F, Boggiani D et al.EGFR and EML4–ALK gene mutations in NSCLC: a case report of erlotinib-resistant patient with both concomitant mutations. Lung Cancer71(2), 241–243 (2011).
   PubMedGoogle Scholar
• Kuo YW, Wu SG, Ho CC et al. Good response to gefitinib in lung adenocarcinoma harboring coexisting EML4–ALK fusion gene and EGFR mutation. J. Thorac. Oncol.5, 2039–2040 (2010).
   PubMedGoogle Scholar
• Korpanty G, Mulligan N, Carney DN. Complete radiological response of metastatic anaplastic lymphoma kinase-positive signet ring lung adenocarcinoma to systemic chemotherapy. J. Thorac. Oncol.6, 963–965 (2011).
   Google Scholar
• Hirsch FR, Wynes MW, Gandara DR et al. The tissue is the issue: personalized medicine for non-small cell lung cancer. Clin. Cancer Res.16, 4909–4911 (2010).
   PubMed Web of Science ®Google Scholar
• Takeuchi K, Choi YL, Soda M et al. Multiplex reverse transcription-PCT screening for EML4–ALK fusion transcripts. Clin. Cancer Res.14, 6618–6624 (2008).
   PubMed Web of Science ®Google Scholar
• Christensen JG, Zou HY, Arango ME et al. Cytoreductive antitumor acitivity of PF-2341066, a novel inhibitor of anaplastic lymphoma kinase and c-MET, in experimental models of anaplastic large-cell lymphoma. Mol. Cancer Ther.6, 3314–3322 (2007).
   PubMed Web of Science ®Google Scholar
• McDermott U, Iafrate AJ, Gray NS et al. Genomic alterations of anaplastic lymphoma kinase may sensitize tumors to anaplastic lymphoma kinase inhibitors. Cancer Res.68, 3389–3395 (2008).
   PubMed Web of Science ®Google Scholar
• Camidge DR, Bang YJ, Iafrate AJ et al. Clinical activity of crizotinib (PF-02341066), in ALK-positive patients with advanced non-small cell lung cancer. Presented at: 35th European Society for Medical Oncology Congress. Milan, Italy, 8–12 October 2010.
   Google Scholar
• Solomon B, Bang YJ, Camidge DR et al. Timing of responses to crizotinib (PF-02341066) in anaplastic lymphoma kinase (ALK)-positive patients with advanced non-small cell lung cancer (NSCLC). Presented at: 22nd EORTC-NCI-AACR Symposium on Molecular Target and Cancer Theraputics. Berlin, Germany, 16–19 November 2010.
   Google Scholar
• Choi YL, Soda M, Yamashita Y et al.EML4–ALK mutations in lung cancer that confer resistance to ALK inhibitors. N. Engl. J. Med.363(18), 1734–1739 (2010).
   PubMed Web of Science ®Google Scholar
• Gerber DE, Minna JD. ALK inhibition for non-small cell lung cancer: from discovery to therapy in record time. Cancer Cell.18, 548–551 (2010).
   PubMed Web of Science ®Google Scholar
• Hallberg B, Palmer RH. Crizotinib – latest champion in the cancer wars? N. Engl. J. Med.363(18), 1760–1762 (2010).
   PubMed Web of Science ®Google Scholar
• Perner S, Wagner PL, Demichelis F et al.EML4–ALK fusion lung cancer: a rare acquired event. Neoplasia10, 298–302 (2008).
   PubMed Web of Science ®Google Scholar
• Zhang S, Wang F, Keats J et al. AP26113, a potent ALK inhibitor, overcomes mutations in EML4–ALK that confer resistance to PF-02341066. Presented at: AACR 101st Annual Meeting. Washington, DC, USA, 17–21 April 2010.
   Google Scholar
• Li Y, Ye X, Liu J et al. Evaluation of EML4–ALK fusion proteins in non-small cell lung cancer using small molecule inhibitors. Neoplasia13, 1–11 (2011).
   PubMed Web of Science ®Google Scholar
• Chen Z, Sasaki T, Tan X et al. Inhibition of ALK, PI3K/MEK, and HSP90 in murine lung adenocarcinoma induced by EML4–ALK fusion oncogene. Cancer Res.70, 9827–9836 (2010).
   PubMed Web of Science ®Google Scholar
• Sequist LV, Gettinger S, Senzer NN et al. Activity of IPI-504, a novel heat-shock protein 90 inhibitor, in patients with molecularly defined non-small-cell lung cancer. J. Clin. Oncol.28, 4953–4960 (2010).
   PubMed Web of Science ®Google Scholar
• Normant E, Paez G, West KA et al. The Hsp90 inhibitor IPI-504 rapidly lowers EML4–ALK levels and induces tumor regression in ALK-driven NSCLC models. Oncogene30(22), 2581–2586 (2011).
   PubMed Web of Science ®Google Scholar
• Katayama R, Khan TM, Benes C et al. Therapeutic strategies to overcome crizotinib resistance in non-small cell lung cancers harboring the fusion oncogene EML4–ALK. Proc. Natl Acad. Sci. USA108(18), 7535–7540 (2011).
   PubMed Web of Science ®Google Scholar