AI Article Synopsis

  • Compound mutations in the EGFR gene, particularly in lung adenocarcinoma, lead to poor responses to standard EGFR-tyrosine kinase inhibitors (TKIs).
  • A patient with a compound EGFR mutation (L858R/A871G) experienced rapid progression on erlotinib but responded well to icotinib, suggesting that different EGFR-TKIs may be effective depending on the specific mutation.
  • This case highlights the importance of recognizing diverse responses to various EGFR-TKIs and underscores the need for further research into how these mutations affect treatment outcomes.

Article Abstract

Compound epidermal growth factor receptor (EGFR) mutations are defined as double or multiple independent mutations of the EGFR tyrosine kinase domain (TKD), in which an EGFR-tyrosine kinase inhibitor (TKI)-sensitizing mutation is identified together with a mutation of unclarified clinical significance. Lung adenocarcinoma with compound EGFR mutation shows poor clinical response to EGFR-TKIs. Kobayashi et al. reported a non-small-cell lung cancer (NSCLC) patient whose tumor had EGFR exon21 L858R/A871G mutation presented rapid disease progression to erlotinib. However, in this case, we present an EGFR exon21 L858R/A871G mutation patient exerted significant benefit to icotinib, another first-generation EGFR-TKI, indicating that different EGFR-TKIs have diversiform sensitive sites and therapeutic effects, consistent mutation sites might achieve heterogeneous benefits from different EGFR-TKIs. Our case report provides promising EGFR-TKI for clinical treatment with EGFR exon21 L858R/A871G mutation in NSCLC. More dedicated efforts are needed to clarify their biologic effects on disease course and drug responsiveness.

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Source
http://dx.doi.org/10.1007/s10637-021-01108-3DOI Listing

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