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Editorial
. 2009 Sep 10;27(26):4232-5.
doi: 10.1200/JCO.2009.23.6661. Epub 2009 Aug 10.

EML4-ALK: honing in on a new target in non-small-cell lung cancer

Leora Horn, William Pao
Editorial

EML4-ALK: honing in on a new target in non-small-cell lung cancer

Leora Horn et al. J Clin Oncol. .
No abstract available

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Conflict of interest statement

AUTHORS’ DISCLOSURES OF POTENTIAL CONFLICTS OF INTEREST

Although all authors completed the disclosure declaration, the following author(s) indicated a financial or other interest that is relevant to the subject matter under consideration in this article. Certain relationships marked with a “U” are those for which no compensation was received; those relationships marked with a “C” were compensated. For a detailed description of the disclosure categories, or for more information about ASCO’s conflict of interest policy, please refer to the Author Disclosure Declaration and the Disclosures of Potential Conflicts of Interest section in Information for Contributors.

Figures

Fig 1.
Fig 1.
Schematic representation of EML4-ALK translocations in non–small-cell lung cancer (NSCLC). Multiple EML4-ALK variants (V1 to V7) have been identified in NSCLCs. All involve the intracellular tyrosine kinase domain of anaplastic lymphoma kinase (ALK) starting at a portion encoded by exon 20. EML4, however, is variably truncated. Variant 1 fuses exon 13 to ALK; variant 2 fuses exon 20; variants 3a and 3b fuse exon 6a and 6b, respectively; variant 4 fuses exon 14 (with an additional 11 nucleotides of unknown origin [dark blue] and starting at nucleotide 50 in exon 20); variants 5a and 5b fuse exon 2 (with 5b containing an additional 117 nucleotides from intron 19); variant 6 fuses exon 13 (with an additional 69 nucleotides from intron 19 [dark blue]); and variant 7 fuses exon 14 (starting at nucleotide 13 in exon 20). Additional variants have been reported as V4, fusing exon 15 (minus 19 nucleotides and starting at nucleotide 21 in exon 20), and V5, fusing exon 18. The nomenclatures used in the literature are depicted on the right. On the left is another potential nomenclature, slightly modified from that of Hiroyoki Mano (see http://atlasgeneticsoncology.org/Tumors/inv2p21p23NSCCLunglD5667.html).
Fig 2.
Fig 2.
Suggested algorithm for molecular testing for patients with non–small-cell lung cancer with tumors of adenocarcinoma histology before treatment with oral targeted therapy. (*) “Other” includes BRAF, MEK1, AKT1, PIK3CA, and so on.
See this image and copyright information in PMC

Comment on

References

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