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Activation of KRAS mediates resistance to targeted therapy in MET exon 14 mutant non-small cell lung cancer
PURPOSE: MET exon 14 splice site alterations that cause exon skipping at the mRNA level (METex14) are actionable oncogenic drivers amenable to therapy with MET tyrosine kinase inhibitors (TKI); however, secondary resistance eventually arises in most cases while other tumors display primary resistanc...
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| Udgivet i: | Clin Cancer Res |
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| Main Authors: | , , , , , , , , , , , , , , , , , |
| Format: | Artigo |
| Sprog: | Inglês |
| Udgivet: |
2018
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| Fag: | |
| Online adgang: | https://ncbi.nlm.nih.gov/pmc/articles/PMC6377821/ https://ncbi.nlm.nih.gov/pubmed/30352902 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1158/1078-0432.CCR-18-1640 |
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