ReviewBiochemical Society transactions2025
Mechanistic insights into MET exon 14 skipping mutations and their role in tumor progression.
Review in Biochemical Society transactions, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed.
- The Role of Alternative Splicing in Lung Cancer: Mechanisms, Regulators, and Therapeutic Implications.International journal of molecular sciences · 2026Review
- Functional Depth Biomarkers Distinguish Lung Squamous Cell Carcinoma from Lung Adenocarcinoma.Research square · 2026Article
- Targeting MET in 2025: From Exon 14 Skipping to MET-Amplified Acquired Resistance in Non-Small Cell Lung Cancer.International journal of molecular sciences · 2026Review
- [Chinese Expert Consensus on Diagnosis and Treatment of Non-small Cell Lung Cancer with MET Abnormality (2026 Version)].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2026Review
- Association of MUC3A P258S mutation with advanced phase CML structural and in silico insights.Functional & integrative genomics · 2026Article
- Clinical response in advanced non-small cell lung cancer with high PD-L1 expression andFrontiers in oncology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The MET receptor tyrosine kinase is a pivotal regulator of cellular survival, motility, and proliferation. Mutations leading to skipping of exon 14 (METΔex14) within the juxtamembrane domain of MET impair receptor degradation and prolong oncogenic signaling, contributing significantly to tumor progression across multiple cancer types. METΔex14 mutations are associated with aggressive clinical behavior, therapeutic resistance, and poor outcomes. Next-generation sequencing from both tissue and liquid biopsies has significantly improved the detection frequency of METΔex14 in lung and other cancers. However, clinical trials targeting METΔex14 have rendered partial responses and mixed outcomes due to the lack of a comprehensive mechanistic understanding of METΔex14 regulation and a diverse mutational landscape. This review synthesizes current knowledge on the mechanistic basis of METΔex14-driven oncogenesis, including alterations in receptor dynamics, downstream signaling perturbations, genomic alterations underlying this mutation, and mechanisms of acquired therapeutic resistance. We further discuss the clinical implications of these insights and highlight future research directions essential for optimizing targeted therapies.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.