| Literature DB >> 24316558 |
Fei-fei Teng1, Jian-dong Zhang2, Xue Meng1, Jin-ming Yu1.
Abstract
Epidermal growth factor receptor (EGFR) mutations in patients with non-small cell lung cancer (NSCLC) usually develop disease progression after a median of 10 to 14 mo on tyrosine kinase inhibitor (TKI). Several mechanisms of resistance to TKI have been described, threonine-methionine substitution at position 790 (T790M), mesenchymal-epithelial transition factor (MET) amplification, overexpression of hepatocyte growth factor (HGF), upregulation of insulin-like growth factor (IGF) receptor signaling, transformation to small cell lung cancer, and so on. A variety of different therapeutic approaches aimed at overcoming resistance are motivated, irreversible EGFR inhibitors, combination with EGFR targeted antibodies, mesenchymal-epithelial transition factor (MET) inhibitors, HGF inhibitors, and so forth. Nevertheless, the results were not optimistic. Here we report a case of reversion of erlotinib-acquired resistance twice, and had a good improvement of outcomes every time. There are some possible reasons for this phenomenon. Considering this report, the patients who acquired resistance after retreatment of EGFR-TKI, using EGFR-TKI repeatedly may be a choice selectively.Entities:
Keywords: EGFR-TKI; NSCLC; erlotinib; gemcitabine; resistance
Mesh:
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Year: 2013 PMID: 24316558 PMCID: PMC3928132 DOI: 10.4161/cbt.27221
Source DB: PubMed Journal: Cancer Biol Ther ISSN: 1538-4047 Impact factor: 4.742