Editorial
Concomitant ALK/KRAS and ALK/EGFR mutations in non small cell lung cancer: different profile of response to target therapies
Abstract
The development of therapeutic agents targeting products of epidermal growth factor receptor (EGFR) gene mutation and anaplastic lymphoma kinase (ALK) rearrangements has significantly improved survival in patients with non small cell lung cancer (NSCLC). Thus, the patients eligible for the treatment with EGFR or ALK inhibitors should be selected through appropriate molecular tests (1). On the other hand, although representing the most frequent genic alteration in NSCLC patients, Kirsten rat sarcoma viral oncogene homolog (KRAS) mutation-specific therapy has not been validated in clinical practice (2). Indeed KRAS mutations are described in approximately 20–30% of NSCLC, commonly observed in smokers and associated with a poor prognosis (2).