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Identification of the transforming EML4–ALK fusion gene in non-small-cell lung cancer

Author

Listed:
  • Manabu Soda

    (Division of Functional Genomics,
    Division of Pulmonary Medicine,)

  • Young Lim Choi

    (Division of Functional Genomics,)

  • Munehiro Enomoto

    (Division of Functional Genomics,
    Division of Pulmonary Medicine,)

  • Shuji Takada

    (Division of Functional Genomics,)

  • Yoshihiro Yamashita

    (Division of Functional Genomics,)

  • Shunpei Ishikawa

    (Research Center for Advanced Science and Technology, University of Tokyo, Tokyo 153-8904, Japan)

  • Shin-ichiro Fujiwara

    (Division of Functional Genomics,)

  • Hideki Watanabe

    (Division of Functional Genomics,)

  • Kentaro Kurashina

    (Division of Functional Genomics,)

  • Hisashi Hatanaka

    (Division of Functional Genomics,)

  • Masashi Bando

    (Division of Pulmonary Medicine,)

  • Shoji Ohno

    (Division of Pulmonary Medicine,)

  • Yuichi Ishikawa

    (The Cancer Institute, Japanese Foundation for Cancer Research, Tokyo 135-8550, Japan)

  • Hiroyuki Aburatani

    (Research Center for Advanced Science and Technology, University of Tokyo, Tokyo 153-8904, Japan
    Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Agency, Saitama 332-0012, Japan)

  • Toshiro Niki

    (and)

  • Yasunori Sohara

    (Jichi Medical University, Tochigi 329-0498, Japan)

  • Yukihiko Sugiyama

    (Division of Pulmonary Medicine,)

  • Hiroyuki Mano

    (Division of Functional Genomics,
    Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Agency, Saitama 332-0012, Japan)

Abstract

Improvement in the clinical outcome of lung cancer is likely to be achieved by identification of the molecular events that underlie its pathogenesis. Here we show that a small inversion within chromosome 2p results in the formation of a fusion gene comprising portions of the echinoderm microtubule-associated protein-like 4 (EML4) gene and the anaplastic lymphoma kinase (ALK) gene in non-small-cell lung cancer (NSCLC) cells. Mouse 3T3 fibroblasts forced to express this human fusion tyrosine kinase generated transformed foci in culture and subcutaneous tumours in nude mice. The EML4–ALK fusion transcript was detected in 6.7% (5 out of 75) of NSCLC patients examined; these individuals were distinct from those harbouring mutations in the epidermal growth factor receptor gene. Our data demonstrate that a subset of NSCLC patients may express a transforming fusion kinase that is a promising candidate for a therapeutic target as well as for a diagnostic molecular marker in NSCLC.

Suggested Citation

  • Manabu Soda & Young Lim Choi & Munehiro Enomoto & Shuji Takada & Yoshihiro Yamashita & Shunpei Ishikawa & Shin-ichiro Fujiwara & Hideki Watanabe & Kentaro Kurashina & Hisashi Hatanaka & Masashi Bando , 2007. "Identification of the transforming EML4–ALK fusion gene in non-small-cell lung cancer," Nature, Nature, vol. 448(7153), pages 561-566, August.
    • Handle: RePEc:nat:nature:v:448:y:2007:i:7153:d:10.1038_nature05945
    DOI: 10.1038/nature05945
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