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• W2014719020 abstract "A 40-year-old man who had complained of bloody sputum was referred to our hospital for workup. Chest computed tomography showed a significant mediastinal lymphadenopathy (Figure 1A). Bronchoscopic examination revealed a tumor compressing the right mainstem bronchus (Figure 2A). Massive bleeding from the tumor was caused by passage of the bronchoscope. Therefore, a diagnosis of pulmonary adenocarcinoma was made by sputum cytology. The patient first received conventional chemotherapy in the form of four courses of cisplatin plus vinorelbine (CDDP + VNR), two cycles of cisplatin plus gemcitabine (CDDP + GEM), and four cycles of carboplatin plus gemcitabine (CBDCA + GEM). However, both the size of the tumor and the serum carcinoembryonic antigen level continued to increase. Fluorodeoxyglucose positron emission tomography suggested systemic metastasis in hilar and mediastinal lymph nodes and bone (Figure 1B).FIGURE 2A, Bronchoscopic examination showed tumor compression of the right main bronchus, and the tumor had hyperplastic vessels on its surface. B, EBUS-TBNA was performed for a pretracheal lymph node (#2R). C, Histologic core revealed metastatic adenocarcinoma in #2R node. D, Immunohistochemistry was positive for ALK protein using the iAEP method. E, FISH revealed the EML4-ALK fusion gene. EML4-ALK split assay with labeled probes for the upstream (red) and downstream (green, arrow) region of the ALK locus. EML4-ALK fusion assay with labeled probes for EML4 (green, arrow) or ALK (red, arrow). Fusion gene showed EML4-ALK (arrow). F, RT-PCR using specific primer set for each variant also confirmed the presence of EML4-ALK variant 1 (274bp). The presence of variant 1 type fusion was also confirmed by direct sequence of the RT-PCR product (data not shown). RT-PCR, reverse transcriptase-polymerase chain reaction; FISH, fluorescence in situ hybridization.View Large Image Figure ViewerDownload (PPT) We performed endobronchial ultrasound-guided transbronchial needle aspiration (EBUS-TBNA) to avoid bleeding from the tumor. Metastatic adenocarcinoma was revealed in an upper paratracheal lymph node (#2R) (Figures 2B, C). Because the epidermal growth factor receptor gene was wild type, we examined the presence of ALK fusion genes. Immunohistochemistry by the intercalated antibody-enhanced polymer (iAEP) method1Inamura 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. 2009; 22: 508-515Crossref PubMed Scopus (386) Google Scholar showed an expression of ALK protein in the samples obtained by EBUS-TBNA (Figure 2D). EML4-ALK fusion gene was also confirmed by both fluorescence in situ hybridization (Figure 2E) and reverse transcriptase-polymerase chain reaction (Figure 2F). Direct sequencing of the PCR product revealed the presence of EML4-ALK variant 1. Thus, we referred the patient for enrollment in a clinical trial with crizotinib (PF-02341066).2Bang Y Kwak EL Shaw AT et al.Clinical activity of the oral ALK inhibitor PF-02341066 in ALK-positive patients with non-small cell lung cancer (NSCLC).J Clin Oncol. 2010; 28 (Abstract 3.)Google Scholar Six weeks after administration of the crizotinib (250 mg twice a day, oral administration), the bloody sputum disappeared, and the tumor size decreased on chest computed tomography (Figure 1C). The carcinoembryonic antigen level also normalized. Five months after administration, an abnormal accumulation almost disappeared on fluorodeoxyglucose positron emission tomography scan (Figure 1D). The observed side effects were only slight nausea during the early period of administration. The patient remains in good condition without tumor relapse for 10 months. The patient suddenly complained bilateral lower extremities paralysis, and the spinal cord metastasis was revealed. The patient was discontinued treatment during the trial in April 2010 because of disease progression. Fusion of ALK with EML4 gives rise to a highly potent oncogene in non-small cell lung cancer,3Soda M Choi YL Enomoto M et al.Identification of the transforming EML4-ALK fusion gene in non-small-cell lung cancer.Nature. 2007; 448: 561-566Crossref PubMed Scopus (3945) Google Scholar being detected in ∼5% of all non-small cell lung cancer cases.1Inamura 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. 2009; 22: 508-515Crossref PubMed Scopus (386) Google Scholar, 3Soda M Choi YL Enomoto M et al.Identification of the transforming EML4-ALK fusion gene in non-small-cell lung cancer.Nature. 2007; 448: 561-566Crossref PubMed Scopus (3945) Google Scholar, 4Takeuchi 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. 2009; 15: 3143-3149Crossref PubMed Scopus (594) Google Scholar Presence of the ALK fusions can be detected by immunohistochemical screening4Takeuchi 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. 2009; 15: 3143-3149Crossref PubMed Scopus (594) Google Scholar and can be also confirmed by fluorescence in situ hybridization and reverse transcriptase-polymerase chain reaction.4Takeuchi 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. 2009; 15: 3143-3149Crossref PubMed Scopus (594) Google Scholar Recently, with progress in chemotherapeutic research, molecular targeted therapeutic agents have been developed, including ALK kinase inhibitors that are now being clinically tested.2Bang Y Kwak EL Shaw AT et al.Clinical activity of the oral ALK inhibitor PF-02341066 in ALK-positive patients with non-small cell lung cancer (NSCLC).J Clin Oncol. 2010; 28 (Abstract 3.)Google Scholar Ideally, ALK fusion gene assessment should be performed using minimally invasive means to obtain biopsy samples sufficient for genetic analysis for subsequent targeted molecular therapy. Histologic as well as cytologic samples can be obtained by EBUS-TBNA, and we have previously reported that high-quality cores are adequate for molecular analyses for biomarkers.5Nakajima T Yasufuku K Suzuki M et al.Assessment of epidermal growth factor receptor mutation by endobronchial ultrasound-guided transbronchial needle aspiration.Chest. 2007; 132: 597-602Crossref PubMed Scopus (182) Google Scholar The dramatic effect of the ALK inhibitor in this patient demonstrates that adequate biomarker assessment contributes to the optimum selection of reagents in targeted molecular therapy and in individualized treatment. Supported, in part, by the Ministry of Education, Culture, Sports, Science and Technology, Grant-in-Aid for Young Scientists (B) No. 21791340 in 2009 (to T.N.), and Grant-in-Aid for Cancer Research from Ministry of Health, Labor and Welfare in 2009 (to T.N.). The authors are grateful to Dr. Yung-Jue Bang (Seoul National University) for the treatment of this patient. They also thank Mr. Hajime Kageyama for support of molecular analysis." @default.
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• W2014719020 title "Treatment of Lung Cancer with an ALK Inhibitor After EML4-ALK Fusion Gene Detection Using Endobronchial Ultrasound-Guided Transbronchial Needle Aspiration" @default.
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