Hepatic metastasis is a poor predictive marker for erlotinib in lung adenocarcinoma

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• 作者：Yayi He^a ; ¹ ; Yan Wang^a ; ¹ ; Shijia Zhang^a ; Shengxiang Ren^a ; Jiayu Li^b ; Caicun Zhou^a ; ^{caicunzhoudr@163.com" class="auth_mail" title="E-mail the corresponding author}
• 刊名：Medical Hypotheses
• 出版年：2016
• 出版时间：September 2016
• 年：2016
• 卷：94
• 期：Complete
• 页码：20-22
• 全文大小：234 K

文摘

Lung cancer is the leading cause of cancer related death worldwide and most of lung cancer patients have had metastases when they are diagnosed. With respect to chemotherapy, target therapy is a more effective and less toxic treatments. The epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs), such as gefitinib or erlotinib, are one of the representatives of targeted therapy which have been widely used in first line, maintenance and 2nd/3rd line therapy among advanced non-small cell lung cancer (NSCLC). But those with hepatic metastases may insensitive to EGFR-TKIs due to MET activation by hepatocyte growth factor (HGF).

In our retrospective analysis, 164 lung adenocarcinoma patients with known epidermal growth factor receptor (EGFR) mutation status who received the treatment of erlotinib as 2nd/3rd line setting were reviewed. The disease control rate (DCR) in patients without hepatic metastases group was higher than that in patients with hepatic metastases (66.1% vs 54.5%, p < 0.001). In EGFR mutation-positive patients, median PFS was significantly longer in patients without hepatic metastases than that in those with hepatic metastases (9.9 months 95% CI 7.74–12.06 months vs. 7.9 months 95% CI 5.88–9.92 months; p = 0.017). Therefore, we assume that hepatic metastasis may be a poor predictive marker for erlotinib in lung adenocarcinoma.