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• W4321166556 abstract "Exon skipping mutations of the MET receptor tyrosine kinase (METex14), increasingly reported in cancers, occur in 3-4% of non-small-cell lung cancer (NSCLC). Only 50% of patients have a beneficial response to treatment with MET-tyrosine kinase inhibitors (TKIs), underlying the need to understand the mechanism of METex14 oncogenicity and sensitivity to TKIs. Whether METex14 is a driver mutation and whether it requires hepatocyte growth factor (HGF) for its oncogenicity in a range of in vitro functions and in vivo has not been fully elucidated from previous preclinical models. Using CRISPR/Cas9, we developed a METex14/WT isogenic model in nontransformed human lung cells and report that the METex14 single alteration was sufficient to drive MET-dependent in vitro anchorage-independent survival and motility and in vivo tumorigenesis, sensitising tumours to MET-TKIs. However, we also show that human HGF (hHGF) is required, as demonstrated in vivo using a humanised HGF knock-in strain of mice and further detected in tumour cells of METex14 NSCLC patient samples. Our results also suggest that METex14 oncogenicity is not a consequence of an escape from degradation in our cell model. Thus, we developed a valuable model for preclinical studies and present results that have potential clinical implication." @default.
• W4321166556 created "2023-02-18" @default.
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• W4321166556 date "2023-07-14" @default.
• W4321166556 modified "2023-09-30" @default.
• W4321166556 title "<scp>MET</scp> exon 14 skipping mutation is a hepatocyte growth factor (<scp>HGF</scp>)‐dependent oncogenic driver <i>in vitro</i> and in humanised <i>HGF</i> knock‐in mice" @default.
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• W4321166556 doi "https://doi.org/10.1002/1878-0261.13397" @default.
• W4321166556 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/36799689" @default.
• W4321166556 hasPublicationYear "2023" @default.
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