Oncotarget published "Correlation between PD-L1 expression and MET gene amplification in patients with advanced non-small cell lung cancer and no other actionable oncogenic driver" which reported that herein, the authors investigated the relation between MET gene amplification and PD-L1 expression in patients with advanced NSCLC and no other actionable oncogenic driver.
PD-L1 expression was not significantly different when analyzed by sex, smoking history, and Eastern Cooperative Oncology Group Performance Status Overall survival rates were not significantly affected by MET amplification nor PD-L1 expression.
In conclusion, a positive correlation was found between MET gene amplification and PD-L1 expression and highly expressed in patients with NSCLC and no other actionable oncogenic driver.
A positive correlation was found between MET gene amplification and PD-L1 expression and highly expressed in patients with NSCLC and no other actionable oncogenic driver
Dr. Enric Carcereny from The Catalan Institute of Oncology Badalona as well as The Badalona Applied Research Group in Oncology (BARGO) said, "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. The vast majority of primary lung cancers are non-small cell lung cancer. 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.
In cases treated with EGFR-targeting tyrosine kinase inhibitors, a common resistance mechanism occurs through the activation of the MET proto-oncogene, also considered an oncogenic driver. In NSCLC, MET can either be activated through MET gene amplification, with a prevalence of 1–5%, or exon 14 skipping mutations, occurring in around 3% of NSCLCs. The receptor tyrosine kinase encoded by MET is c-MET, whose ligand is the hepatocyte growth factor. Therefore, immunotherapy with anti-PD-1 and anti-PD-L1 agents has yielded positive results in patients with advanced NSCLC.
Figure 5: Kaplan-Meier curve of overall survival of patients overexpressing PD-L1 (orange line) and not overexpressing PD-L1 (blue line). Median overall survival of the group overexpressing PD-L1 (> 50%): 8 months (95% CI: 4.0–11.9). Median overall survival of the group not overexpressing PD-L1 (≤ 50%): 38 months (95% CI: 0–NR; p-value = 0.893).
Several studies have proven that PD-L1 expression is correlated with wild-type EGFR, ROS1 rearrangement, and erlotinib-resistant NSCLC, while it is not associated with ALK mutations.
Besides, in some of these studies, MET gene amplification up-regulated PD-L1 expression, especially correlating with PD-L1 overexpression—considered as such for a tumor proportion score > 50% .
The Carcereny Research Team concluded in their Oncotarget Research Output, "a positive correlation was found between MET gene amplification and PD-L1 expression and overexpression in patients with NSCLC and no other actionable oncogenic driver. In our study, PD-L1 expression was not affected by sex, PS, or smoking history, and PD-L1 expression and MET gene amplification did not affect the OS rates of our cohort. Further studies are needed to appraise the impact this finding may have on possible treatments for these patients."
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DOI - https://doi.org/10.18632/oncotarget.28045
Full text - https://www.oncotarget.com/article/28045/text/
Correspondence to - Enric Carcereny - [email protected]
Keywords - non-small cell lung cancer, oncogenic driver, PD-L1, MET amplification, smoking habit
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