New data on clinical decisions in NSCLC patients with uncommon EGFR mutations

ABSTRACT

Introduction: Non-small cell lung cancer patients harboring uncommon epidermal growth factor receptor (EGFR) mutations together account for approximately 10% of all EGFR mutations. The most common of which being G719X, S768I, L861Q, and exon 20 insertions. The clinical significance, particularly their response to EGFR tyrosine kinase inhibitors (TKIs) is largely unclear. Previous data is limited to a small fraction of patients in prospective studies and retrospective series. Recently, a combined analysis of patients with uncommon EGFR mutations in the Lux-Lung 2, Lux-Lung 3, Lux-Lung 6 trials provide new perspectives of uncommon EGFR mutations.

Areas covered: This review reports the existing evidence from major prospective and retrospective studies, along with new data that focus on the clinical significance of uncommon EGFR mutations.

Expert commentary: The clinical data of uncommon EGFR mutations should be interpreted carefully as data from prospective and retrospective studies are not considered at the same level of evidence.

KEYWORDS:

• Non-small cell lung cancer
• uncommon EGFR mutation
• tyrosine kinase inhibitor
• G719X
• L861Q
• S768I
• exon 20 insertions

Declaration of interest

JC. Yang received honorarium for speeches or participated on a compensated advisory board for Boehringer Ingelheim, Eli Lilly, Bayer, Roche/Genentech/Chugai, Astellas, MSD, Merck, Serono, Pfizer, Novartis, Clovis Oncology, Celgene, Merrimack, Yuhan Pharmaceuticals, BMS and Ono Pharmaceutical and participated on an uncompensated advisory board for AstraZeneca. C. Lin is a consultant and received honoraria from Boehringer Ingelheim and Novartis. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

Additional information

Funding

This paper was not funded.