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ECB-ART-50202
Nature 2007 Aug 02;4487153:561-6. doi: 10.1038/nature05945.
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Identification of the transforming EML4-ALK fusion gene in non-small-cell lung cancer.

Soda M , Choi YL , Enomoto M , Takada S , Yamashita Y , Ishikawa S , Fujiwara S , Watanabe H , Kurashina K , Hatanaka H , Bando M , Ohno S , Ishikawa Y , Aburatani H , Niki T , Sohara Y , Sugiyama Y , Mano H .


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.

PubMed ID: 17625570
Article link: Nature