This content was funded by Johnson & Johnson. This material is intended for educational and scientific exchange purposes only. It is not intended to be promotional and should not be used to make treatment decisions for any individual patient. The views expressed are those of the speaker and do not necessarily reflect those of Johnson & Johnson.
Atypical EGFR mutations make up approximately 5–10% of EGFR-mutant non-small cell lung cancer (NSCLC), and because some assays only report exon 19 deletions and L858R, they are easy to miss. In this short podcast, Melina Marmarelis, thoracic oncologist at the University of Pennsylvania, Philadelphia, USA, explains why these mutations often respond differently to EGFR tyrosine kinase inhibitors and how to pick them up on next-generation sequencing (NGS). She also walks through CHRYSALIS-2 Cohort C, which evaluated amivantamab plus lazertinib in patients who were treatment-naive and previously treated.a
Topics covered:
- Why G719X and other atypical mutations alter the ATP-binding pocket differently from exon 19 deletions and L858R
- Which assays can miss atypical mutations, and when broader NGS is needed
- What CHRYSALIS-2 Cohort C evaluated, and the limitations of a single-arm Phase I/Ib study
- How the American Society of Clinical Oncology (ASCO) Living Guideline now addresses atypical EGFR alterations
aAmivantamab plus lazertinib is not approved by the US Food and Drug Administration for the treatment of atypical EGFR-mutated non-small cell lung cancer. This content includes discussion of investigational and unapproved uses. The data presented do not establish safety or efficacy for any unapproved use. Prescribers should consult the full Prescribing Information for approved indications and complete safety information.
Speaker
Melina E. Marmarelis1
1. Associate Professor of Medicine, Division of Hematology-Oncology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, USA
