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MET Exon 14 Skipping Alterations in NSCLC: Current Understanding and Therapeutic Advances

Published Online: December 23rd 2020 Oncology & Hematology Review (US). 2020;16(2): Online ahead of journal publication
Authors: Rashmi Shah, Deepu Alex, Zhaolin Xu
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Abstract:
Overview

Abnormal activation of Mesenchymal Epithelial Transition (MET) receptor tyrosine kinase is associated with oncogenesis. Various underlying mechanisms including alteration, amplification, gene rearrangement and exon skipping in the transcript account for the abnormal MET signaling. One of the critical alterations in MET leading to non-small cell lung carcinoma (NSCLC) is MET exon 14 (METex14) skipping, a driver mutation, which accounts for approximately 3-4% of lung adenocarcinoma. METex14 skipping results in the formation of a functionally active and stable truncated receptor lacking juxtamembrane regulatory domain responsible for MET ubiquitination. Several MET kinase inhibitors have been developed targeting MET receptors and many are in clinical trials. FDA has recently approved capmatinib (Tabrecta) for the treatment of NSCLC with METex14 skipping alteration. In this paper, we review the current understanding of the implications of aberrant MET activation in NSCLC harboring METex14 skipping alteration, available diagnostic options, potential therapies in the pipeline and the future clinical landscape for such alterations.

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**This manuscript has been accepted for publication but not yet copyedited or typeset, and may be subject to minor changes during the production process.**

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Disclosure

Rashmi Shah, Deepu Alex, and Zhaolin Xu have no financial or non-financial relationships or activities to declare in relation to this article.

Compliance With Ethics

This article involves a review of the literature and did not involve any studies with human or animal subjects performed by any of the authors.

Review Process

Double-blind peer review.

Authorship

The named authors meet the International Committee of Medical Journal Editors (ICMJE) criteria for authorship of this manuscript, take responsibility for the integrity of the work as a whole, and have given final approval for the version to be published.

Correspondence

Zhaolin Xu, MD, Department of Anatomical Pathology, Queen Elizabeth II Health Science Centre, 5788 University Ave. Rm 734, Halifax B3H 1V8, NS, Canada

E: zhaolin.xu@nshealth.ca

Support

No funding was received in the publication of this article.

Open Access

This article is freely accessible at touchONCOLOGY.com © Touch Medical Media 2020.

Received

2020-10-14

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