These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Acquired Resistance to Crizotinib in NSCLC with MET Exon 14 Skipping.
    Author: Heist RS, Sequist LV, Borger D, Gainor JF, Arellano RS, Le LP, Dias-Santagata D, Clark JW, Engelman JA, Shaw AT, Iafrate AJ.
    Journal: J Thorac Oncol; 2016 Aug; 11(8):1242-1245. PubMed ID: 27343442.
    Abstract:
    INTRODUCTION: MET proto-oncogene, receptor tyrosine kinase gene (MET) exon 14 skipping is a targetable alteration in lung cancer. Treatment with MET proto-oncogene, receptor tyrosine kinase inhibitor can cause dramatic responses in patients whose cancers have MET exon 14 skipping. Little is known, however, about acquired resistance in patients with MET exon 14 skipping. METHODS: Biopsy specimens obtained at baseline and at the time of progression for a patient being treated with crizotinib were compared using targeted next-generation sequencing to assess for mechanisms of resistance. RESULTS: An acquired mutation in the MET kinase domain, D1228N, was found at time of progression on crizotinib in a patient with MET exon 14 skipping. CONCLUSIONS: One potential mechanism of acquired resistance to crizotinib in patients with MET exon 14 skipping is through second-site mutations in the MET gene. Understanding mechanisms of resistance will be important in optimizing therapy in these patients.
    [Abstract] [Full Text] [Related] [New Search]