Long-term survival with erlotinib in advanced lung adenocarcinoma harboring synchronous EGFR G719S and KRAS G12C mutations

• Published in: Lung cancer (Amsterdam, Netherlands) Vol. 120; pp. 70 - 74
• Main Authors: Ricciuti, Biagio, Baglivo, Sara, Ludovini, Vienna, Sidoni, Angelo, Metro, Giulio, Brambilla, Marta, Siggillino, Annamaria, Reda, Maria Sole, Rebonato, Alberto, Maiettini, Daniele, Chiari, Rita
• Format: Journal Article
• Language: English
• Published: Ireland Elsevier B.V 01.06.2018
• Subjects: Adenocarcinoma - drug therapy; Adenocarcinoma - genetics; Adenocarcinoma - mortality; Antineoplastic Agents - therapeutic use; Disease Progression; DNA Mutational Analysis - methods; EGFR; ErbB Receptors - genetics; Erlotinib; Erlotinib Hydrochloride - therapeutic use; Humans; KRAS; Lung Neoplasms - drug therapy; Lung Neoplasms - genetics; Lung Neoplasms - mortality; Male; Mutation - genetics; Neoplasm Staging; NGS; NSCLC; Proto-Oncogene Proteins p21(ras) - genetics; Remission Induction; Survival Analysis; Time Factors; KRAS; NGS; NSCLC; Erlotinib; EGFR
• ISSN: 0169-5002; 1872-8332
• DOI: 10.1016/j.lungcan.2018.04.002

•In NSCLC, EGFR and KRAS mutations rarely coexist.•Multiple mutations are challenging for the decision of TKIs treatment in NSCLC.•A long-term survival (+9 years) with erlotinib in double-mutant NSCLC is reported.•Treatment beyond PD is an efficacious strategy in EGFR-mutant NSCLC patients. Although epidermal growth factor receptor (EGFR) and v-Ki-ras2 Kirsten rat sarcoma viral oncogene (KRAS) mutations were thought to be mutually exclusive in patients with non-small cell lung cancer (NSCLC), the development of high sensitive large-scale mutation analysis, has increasingly shown that activating EGFR mutations occasionally coexist with other dominant genetic alterations. Herein, we discuss the case of a patient with advanced NSCLC harboring both the uncommon EGFR G719S and the KRAS G12C mutations, who was treated for 9 years with erlotinib achieving a long-term survival. In light of their rarity, multiple mutations are very challenging for the decision of tyrosine kinase inhibitors (TKIs) treatment, especially when EGFR mutations occur together with mutations known to provide resistance to EGFR TKIs, such as KRAS.