Monitoring of cyclooxygenase-2 levels can predict EGFR mutations and the efficacy of EGFR-TKI in patients with lung adenocarcinoma.

backgroundEpidermal growth factor receptor (EGFR) mutation detection has become a routine molecular test with significant implications for prognosis and therapeutic options of EGFR tyrosine kinase inhibitors (EGFR-TKIs). However, acquiring sufficient amounts of tissue for analyzing EGFR mutations is not often feasible, and not all the patients with sensitive EGFR mutations have benefit from EGFR-TKI treatment.

methodEGFR mutations were detected by amplification refractory mutation system (ARMS) in 44 patients of newly diagnosed lung adenocarcinoma, and patients with EGFR-positive mutations received EGFR-TKI treatment. The serum cyclooxygenase-2 (COX-2) levels were tested before EGFR-TKI treatment and on the 30th days after EGFR-TKI treatment.

resultsTwenty-nine cases were detected EGFR mutations. EGFR mutation rate of serum COX-2 high-level group was significantly higher than low-level group (92.9% vs. 53.3%, P=0.025). Multivariate analysis showed that serum COX-2 level was independently associated with EGFR mutation (P=0.033, OR=12.385, 95%CI, 1.231-124.567). Analysis of the correlation between clinical characteristics and the response of EGFR-TKI showed that the serum COX-2 high-level group had a better efficacy than low-level group (P=0.000), and multivariate logistic regression analysis showed that the serum COX-2 level was the independently influencing factor (P=0.004). Kaplan-Meier analysis showed that patients of COX-2 high-level group have longer progression-free survival (PFS, P=0.013), and the Cox regression analysis showed that the same result (P=0.003; OR=0.980, 95% CI, 0.967-0.993).

conclusionThe serum COX-2 level seems to be closely associated with EGFR mutations in patients with Lung adenocarcinoma. The serum COX-2 level could help us to predict the responses of EGFR-TKI and the PFS in patients harboring EGFR mutation.