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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Bibliografiset tiedot
Julkaisussa:Clin Cancer Res
Päätekijät: Suzawa, Ken, Offin, Michael, Lu, Daniel, Kurzatkowski, Christopher, Vojnic, Morana, Smith, Roger S., Sabari, Joshua K., Tai, Huichun, Mattar, Marissa, Khodos, Inna, de Stanchina, Elisa, Rudin, Charles M., Kris, Mark G., Arcila, Maria E., Lockwood, William W., Drilon, Alexander, Ladanyi, Marc, Somwar, Romel
Aineistotyyppi: Artigo
Kieli:Inglês
Julkaistu: 2018
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Article
Linkit: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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