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      KIF5B-RET fusions in lung adenocarcinoma

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          Abstract

          We identified in-frame fusion transcripts of KIF5B (the kinesin family 5B gene) and the RET oncogene, which are present in 1–2% of lung adenocarcinomas (LADCs) from people from Japan and the United States, using whole-transcriptome sequencing. The KIF5B-RET fusion leads to aberrant activation of RET kinase and is considered to be a new driver mutation of LADC because it segregates from mutations or fusions in EGFR, KRAS, HER2 and ALK, and a RET tyrosine kinase inhibitor, vandetanib, suppresses the fusion-induced anchorage-independent growth activity of NIH3T3 cells.

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          Author and article information

          Journal
          9502015
          8791
          Nat Med
          Nat. Med.
          Nature medicine
          1078-8956
          1546-170X
          6 January 2019
          12 February 2012
          12 February 2012
          22 March 2019
          : 18
          : 3
          : 375-377
          Affiliations
          [1 ]Division of Genome Biology, National Cancer Center Research Institute, Chuo-ku, Tokyo, Japan.
          [2 ]Division of Genetics, National Cancer Center Research Institute, Chuo-ku, Tokyo, Japan.
          [3 ]Division of Cancer Genomics, National Cancer Center Research Institute, Chuo-ku, Tokyo, Japan.
          [4 ]Department of Metabolic Disorder, Diabetes Research Center, Research Institute, National Center for Global Health and Medicine, Shinjuku-ku, Tokyo, Japan.
          [5 ]Division of Pathology and Clinical Laboratories, National Cancer Center Hospital, Chuo-ku, Tokyo, Japan.
          [6 ]Division of Multistep Carcinogenesis, National Cancer Center Research Institute, Chuo-ku, Tokyo, Japan.
          [7 ]Division of Refractory Cancer Research, National Cancer Center Research Institute, Chuo-ku, Tokyo, Japan.
          [8 ]Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, US National Institutes of Health, Bethesda, Maryland, USA.
          [9 ]Section of Toxicology, Department of Chemical and Biological Working Environment, National Institute of Occupational Health, Oslo, Norway.
          [10 ]Science Solutions Division, Mizuho Information and Research Institute, Chiyoda-ku, Tokyo, Japan.
          [11 ]Statistical Genetics Analysis Division, StaGen, Taito-ku, Tokyo, Japan.
          [12 ]Division of Thoracic Surgery, National Cancer Center Hospital, Chuo-ku, Tokyo, Japan.
          [13 ]Division of Thoracic Oncology, National Cancer Center Hospital, Chuo-ku, Tokyo, Japan.
          [14 ]Cancer Genomics Project, University of Tokyo, Bunkyo-ku, Tokyo, Japan.
          [15 ]These authors equally contributed to this work.
          Author notes

          AUTHOR CONTRIBUTIONS

          RNA sequencing: H.I., K.Y., M.H., T.N. and H.S. Sequence data processing: Y.T., S.C. and I.Y. Molecular biological analyses: T.K., Y.S., R.I., H. Ogiwara, T.O., M.E., A.J.S., H. Okayama, A.H., Y.A. and S.O. Clinical and pathological analyses: K.T., K.F., V.S., S.W., I.S. and H.T. Manuscript writing: T.K., H.I. and T.S. Study design: T.K., H.I., C.C.H., T.Y., J.Y. and T.S.

          Correspondence should be addressed to T.K. ( tkkohno@ 123456ncc.go.jp ).
          Article
          PMC6430196 PMC6430196 6430196 nihpa1000523
          10.1038/nm.2644
          6430196
          22327624
          2e23ab43-2add-418d-8dc8-ee2edf28690d

          Reprints and permissions information is available online at http://www.nature.com/reprints/index.html.

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