Abstract
Long-term use of statins has been reported to reduce the risk of death in patients with lung cancer. This study investigated the effect of statin use among patients with lung cancer receiving epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKIs) therapy. A nationwide, population-based case-control study was conducted using the Taiwan National Health Insurance Research Database. From January 1, 1997 to December 31, 2012, a total of 1,707 statin and 6,828 non-statin matched lung cancer cohorts with EGFR-TKIs treatment were studied. Statin use was associated with a reduced risk of death (HR: 0.58, 95% CI: 0.54–0.62, p < 0.001). In addition, statin use was associated with a significantly longer median progression-free survival (8.3 months, 95% CI: 7.6–8.9 vs. 6.1 months, 95% CI: 6.0–6.4, p < 0.001) and median overall survival (35.5 months, 95% CI: 33.8–38.1 vs. 23.9 months, 95% CI: 23.4–24.7, p < 0.001). In conclusion, statins might potentially enhance the therapeutic effect and increase survival in patients with lung cancer receiving EGFR-TKI therapy.
Highlights
Lung cancer is the most common cause of cancer death worldwide [1]
There was no significant difference in smoking-related disorders, epidermal growth factor (EGFR)-TKI usage, and CT regimens before EGFR-TKI among statin users and non-users
After adjustment for statin use, age, sex, urbanization, income, diabetes mellitus (DM), hypertension, stroke, coronary artery disease (CAD), chronic obstructive pulmonary disease (COPD), smoking-related disorders, CT/RT, EGFR-TKI response, and regimens before EGFR-TKI therapy, an increased risk of death was observed in male patients with lung cancer (HR: 1.28, 95% confidence intervals (CI): 1.21–1.35, p
Summary
Most patients have advanced-stage disease at the initial diagnosis of lung cancer. Patients with non-small cell lung cancer (NSCLC) with specific mutations in the tyrosine kinase domain of the epidermal growth factor (EGFR) gene have favorable clinical outcomes with EGFR tyrosine kinase inhibitor (EGFR-TKI) therapy [4]. All mutations are reported in exons 18, 19, 20, and 21 of EGFR [5] and are most frequently found in lung adenocarcinoma [6]. Missense mutations in exon 21 (L858R) and inframe deletions within exon 19 are the most frequent EGFR-TKI sensitive mutations (80%) in patients with NSCLC [9]. For patients with NSCLC, both mutations are associated with favorable responses to first-line treatment with EGFR-TKIs, such as gefitinib [10], erlotinib [11], and afatinib [12] versus standard chemotherapy
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