IGF1R depletion facilitates MET-amplification as mechanism of acquired resistance to erlotinib in HCC827 NSCLC cells

Samankaltaisia teoksia

• Increased PD-L1 expression in erlotinib-resistant NSCLC cells with MET gene amplification is reversed upon MET-TKI treatment
  Tekijä: Demuth, Christina, et al.
  Julkaistu: (2017)
• MET amplification and epithelial-to-mesenchymal transition exist as parallel resistance mechanisms in erlotinib-resistant, EGFR-mutated, NSCLC HCC827 cells
  Tekijä: Jakobsen, K R, et al.
  Julkaistu: (2017)
• Epithelial-to-mesenchymal transition is a resistance mechanism to sequential MET-TKI treatment of MET-amplified EGFR-TKI resistant non-small cell lung cancer cells
  Tekijä: Clement, Michelle Simone, et al.
  Julkaistu: (2020)
• The role of epithelial to mesenchymal transition in resistance to epidermal growth factor receptor tyrosine kinase inhibitors in non-small cell lung cancer
  Tekijä: Jakobsen, Kristine Raaby, et al.
  Julkaistu: (2016)
• The T790M resistance mutation in EGFR is only found in cfDNA from erlotinib-treated NSCLC patients that harbored an activating EGFR mutation before treatment
  Tekijä: Demuth, Christina, et al.
  Julkaistu: (2018)