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Updated: Nov 8, 2025

Characterizing Exon Skipping Efficiency in DMD Patient Samples in Clinical Trials of Antisense Oligonucleotides
Published on: May 7, 2020
Novel MET exon 14 skipping analogs characterized in non-small cell lung cancer patients: A case study
Minke Shi1, Jing Ma2, Meilin Feng2
1Department of Thoracic Surgery, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, China.
Abstract:
MET exon 14 skipping (METex14) is a validated oncogenic driver in lung cancer and MET tyrosine kinase inhibitors are now available as effective clinical treatments. The majority of known METex14 alterations are typical donor/acceptor splicing or ubiquitination site mutations. Herein, two new METex14 variants were detected in two patients with lung adenocarcinoma by targeted next generation sequencing (NGS). Reverse transcription (RT)-based analysis confirmed that these mutations led to MET exon 14 skipping. Our analysis provided evidence for possible targeted therapy options for patients carrying these MET mutations or similar METex14 analogs.
Insights
Two novel MET exon 14 skipping mutations were identified in lung adenocarcinoma patients. These findings expand the understanding of MET alterations and potential targeted therapy options for lung cancer.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- MET exon 14 skipping (METex14) is a recognized driver in lung cancer.
- MET tyrosine kinase inhibitors represent effective clinical treatments for MET-driven cancers.
- Most known METex14 alterations involve canonical splicing or ubiquitination site mutations.
Observation:
- Targeted next-generation sequencing (NGS) identified two previously undocumented METex14 variants in patients with lung adenocarcinoma.
- Reverse transcription (RT)-based analyses confirmed that these novel mutations induce MET exon 14 skipping.
Findings:
- Discovery of two new METex14 variants in lung adenocarcinoma.
- Confirmation of these variants' ability to cause MET exon 14 skipping through RT-based assays.
Implications:
- Broadens the spectrum of known MET alterations driving lung cancer.
- Suggests potential for targeted therapy in patients with these newly identified MET mutations or similar analogs.
- Highlights the importance of comprehensive genomic profiling for identifying actionable MET alterations.
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