Phase II study of erlotinib as a salvage treatment for non-small-cell lung cancer patients after failure of gefitinib treatment
Phase II study of erlotinib as a salvage treatment for non-small-cell lung cancer patients after failure of gefitinib treatment
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DOI：
10.1093/annonc/mdn423
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发表时间：
2008-12-01
影响因子：
50.5
通讯作者：
Lee, J. -S.
中科院分区：
文献类型：
--
作者：
Lee, D. H.;Kim, S. -W.;Lee, J. -S.
背景：吉非替尼和厄洛替尼均为可逆性表皮生长因子受体酪氨酸激酶抑制剂，但具有不同的药理作用。在吉非替尼治疗非小细胞肺癌(NSCLC)失败后，我们进行了厄洛替尼的II期研究。患者和方法：晚期/转移性非小细胞肺癌患者在接受吉非替尼治疗后，给予厄洛替尼150 mg/d治疗，直至病情进展或出现无法耐受的毒性。结果：2006年9月至2008年1月，共纳入23例患者，所有患者的反应和毒性均可评估。所有患者都从不吸烟，除了一人之外，所有人都患有腺癌。23例患者中，1例部分缓解，1例病情稳定，客观有效率为4.3%，疾病控制率为8.7%。这两名患者分别受益于厄洛替尼6.2个月和7.8个月；两人也都曾受益于先前的吉非替尼治疗。最常见的毒性反应是皮疹和腹泻。结论：在吉非替尼治疗失败后，不应常规给予厄洛替尼，但可以作为更高选择的亚群的选择，特别是那些先前从吉非替尼治疗中受益的患者。肿瘤分子标志物的识别对于了解和克服对吉非替尼的获得性耐药具有重要意义。
Background: Both gefitinib and erlotinib are reversible epidermal growth factor receptor tyrosine kinase inhibitors, but they have somewhat different pharmacological properties. We conducted a phase II study of erlotinib after failure of gefitinib treatment in patients with non-small-cell lung cancer (NSCLC).Patients and methods: Patients with advanced/metastatic NSCLC who had shown disease progression on gefitinib treatment were treated with erlotinib 150 mg/day until disease progression or intolerable toxicity.Results: Between September 2006 and January 2008, a total of 23 patients were enrolled and all were assessable for response and toxicity. All patients were never smokers and all but one had adenocarcinoma. Of these 23 patients, one had a partial response and one stable disease, resulting in an objective response rate of 4.3% and a disease control rate of 8.7%. These two patients benefited from erlotinib for 6.2 months and 7.8 months, respectively; both had also benefited from prior gefitinib therapy. The most common toxic effects were skin rash and diarrhea.Conclusion: Erlotinib should not be given routinely after failure of gefitinib treatment, but can be an option for more highly selected subsets, especially those who had benefited from prior gefitinib treatment. Identification of molecular markers in tumors is important to understand and overcome acquired resistance to gefitinib.