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Updated: Mar 23, 2026

Characterizing Exon Skipping Efficiency in DMD Patient Samples in Clinical Trials of Antisense Oligonucleotides
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Characterizing Exon Skipping Efficiency in DMD Patient Samples in Clinical Trials of Antisense Oligonucleotides

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MET Exon 14 Alterations in Lung Cancer: Exon Skipping Extends Half-Life

Alexander Drilon1

  • 1Thoracic Oncology Service, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York. Weill Cornell Medical College, New York, New York. drilona@mskcc.org.

Clinical Cancer Research : an Official Journal of the American Association for Cancer Research
|March 25, 2016
PubMed

Insights

MET exon 14 alterations cause oncogenic transformation through mechanisms like exon skipping. These specific MET mutations are clinically targetable with MET-directed therapies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • MET exon 14 alterations represent a diverse group of genetic mutations.
  • These alterations can lead to exon 14 skipping and impaired receptor degradation.
  • Such alterations are implicated in oncogenic transformation.

Purpose of the Study:

  • To investigate the nature of MET exon 14 alterations.
  • To understand the mechanisms leading to oncogenic transformation.
  • To highlight the clinical targetability of these alterations.

Main Methods:

  • Analysis of splice acceptor and donor sites.
  • Assessment of receptor degradation pathways.
  • Evaluation of oncogenic transformation markers.

Main Results:

  • MET exon 14 alterations frequently disrupt splicing.
  • Exon 14 skipping was identified as a key consequence.
  • Impaired MET receptor degradation was observed.
  • Oncogenic transformation was linked to these alterations.

Conclusions:

  • MET exon 14 alterations are a significant driver of oncogenesis.
  • These alterations represent a targetable vulnerability in cancer.
  • MET-directed therapies offer a clinical approach for patients with these mutations.

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