Association between PD-l1 expression with driver mutations (ALK, ROSL, EFFR) and Histopathology in non-small cell lung cancer

Lung cancer is the first in the world of cancer deaths and new cancer diagnosis. NSCLC is the most common type of lung cancer. New biomarkers developed in the treatment of NSCLC and new generation cancer therapies started to be used to target driver genes, mutations and immune control points. In our study, the relationship between PD-L1 expression with driver mutations (ALK, ROS1, EGFR) and histopathological diagnosis, gender and smoking status parameters in NSCLC, have been statistically analyzed. For this purpose, 501 cases with at least one driver mutation (ALK, ROS1, EGFR) analyzed PD-L1 expression level diagnosed as NSCLC were analyzed retrospectively. Chi-square, Fisher's exact chi-square and Mann-Whitney U test were used for statistical relationship analysis. There was a significant relationship between PD-L1 expression and EGFR mutation (p=0.000). A significant relationship was found between smoking and driver mutations (Fisher exact Chi-square value respectively; p=0.002, p=0.043, p=0.000). There was a significant relationship between sex and EGFR (p=0.001). Histopathological diagnosis revealed a significant relationship between ALK and EGFR (p=0.007, p=0.001). The prevalence of PD-L1 positivity was higher in EGFR wild type patients. Considering this data, it can be interpreted that the chance of immunotherapy may be higher in EGFR wild type cases and the predictive importance of PD-L1 evaluation is increased for these cases. The incidence of driver mutations in non-smokers was found to be higher compared to the users. The incidence of ALK and EGFR positivity was higher in adenocarcinomas. The incidence of EGFR positive in female cases was higher than in male cases. The prevalence of driver mutations in NSCLC in the Turkish population was determined in parallel with the rates in the literatures. No significant relationship was found between PD-L1 and smoking, sex, histopathology, ALK and ROS1.