Abstract
Non-small cell lung cancers (NSCLC) are the most common type of lung cancer and can be classified according to the presence of mutually exclusive oncogenic drivers. The majority of NSCLC patients present a non-actionable oncogenic driver, and treatment resistance through the amplification of the MET proto-oncogene (MET) or the expression of programmed cell death protein 1 ligand (PD-L1) is common. Herein, we investigated the relation between MET gene amplification and PD-L1 expression in patients with advanced NSCLC and no other actionable oncogenic driver (i.e., EGFR, ALK, ROS1). Our retrospective observational study analyzed data from 48 patients (78% men, median age 66 years) admitted to the Germans Trias i Pujol Hospital, Spain, between July 2015 and February 2019. Patients presenting MET amplification showed a higher proportion of PD-L1 expression (93% vs. 39%; p < 0.001) and overexpression (64% vs. 27%; p = 0.020) than those with non-amplified MET. PD-L1 expression was not significantly different when analyzed by sex (p = 0.624), smoking history (p = 0.429), and Eastern Cooperative Oncology Group Performance Status (p = 0.597) Overall survival rates were not significantly affected by MET amplification (high and intermediate amplification vs low amplification and non-amplificated) (p = 0.252) nor PD-L1 expression (> vs =< 50%) (p = 0.893). In conclusion, a positive correlation was found between MET gene amplification and PD-L1 expression and highly expressed (above 50%) in patients with NSCLC and no other actionable oncogenic driver. It could be translated as new guided-treatment oportunities for these patients.
Highlights
Cancer represents a heavy burden for society as a whole, with a high medical, economic, and psychosocial impact
non-small cell lung cancer (NSCLC) can be classified at the molecular level according to the presence of oncogenic drivers that occur in genes crucial to tumor proliferation and survival
The most prevalent mutations in NSCLCs are seen in epidermal growth factor receptor (EGFR) (10– 15%) followed by rearrangements in anaplastic lymphoma kinase (ALK) (3–7%) and ROS1 (1–2%) genes [2, 3]
Summary
Cancer represents a heavy burden for society as a whole, with a high medical, economic, and psychosocial impact. Lung cancer is one of the most common cancers and has the highest death toll among them; 20% of all cancer-related deaths are attributed to lung cancer [1]. The vast majority of primary lung cancers are non-small cell lung cancer (NSCLC) [1]. NSCLCs can be classified at the molecular level according to the presence of oncogenic drivers that occur in genes crucial to tumor proliferation and survival. Several oncogenic drivers have been identified, which, in most cases, are mutually exclusive from one another [2]. Only a fraction of them are www.oncotarget.com druggable targets, called actionable oncogenic drivers, for which targeted therapies are currently available. Most NSCLC patients present either a nonactionable oncogenic driver or an oncogenic alteration that has not yet been characterized [4, 5]
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