Cetuximab in recurrent and/or metastatic salivary gland carcinomas: A phase II study
Cetuximab in recurrent and/or metastatic salivary gland carcinomas: A phase II study
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DOI：
10.1016/j.oraloncology.2008.07.010
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发表时间：
2009-07-01
期刊：
影响因子：
4.8
通讯作者：
Licitra, L.
中科院分区：
文献类型：
--
作者：
Locati, L. D.;Bossi, P.;Licitra, L.
唾液腺癌中EGFR过表达为研究抗EGFR治疗复发和/或转移性唾液腺癌（RMSGCs）提供了依据。研究西妥昔单抗在临床获益率（CBR）方面的活性，CBR定义为客观反应（CR或PR）或疾病稳定（SD）的发生>= 6个月。2005年4月至12月，30例患者[23例腺样囊性癌（ACC）和7例非ACC]接受西图昔单抗治疗，剂量为400mg /m(2)/周，随后为250mg /m(2)/周，直至病情进展、出现重大毒性或自愿停药。分别采用免疫细胞化学和荧光原位杂交方法回顾性分析EGFR的表达和基因状态。注射西妥昔单抗的中位数为14个疗程（范围5-54）。皮肤毒性是主要的不良事件。西妥昔单抗在50%的病例中提供CBR （95% CL, 31 - 69%）。没有肿瘤样本显示EGFR基因扩增，12%的样本中EGFR拷贝数增加，均为ACC。皮疹>= G2、EGFR过表达、EGFR拷贝数与CB无统计学相关性。在RMSGCs中，进一步评估EGFR靶向药物是可取的，并应通过适当的肿瘤生物学选择进行，以区分ACC与非ACC。(C) 2008 Elsevier Ltd版权所有。
EGFR overexpression in salivary gland carcinomas provides the rational for the investigation of anti-EGFR treatments in recurrent and/or metastatic salivary gland cancers (RMSGCs). The activity of cetuximab in terms of clinical benefit rate (CBR) defined as the occurrence of objective response (CR or PR) or stable disease (SD) for >= 6 months was investigated.From April to December 2005, 30 patients [23 adenoid cystic carcinoma (ACC) and 7 non-ACC] were treated with cetuximab at 400 mg/m(2)/week followed by 250 mg/m(2)/week until progression, major toxicity or voluntary discontinuation. EGFR expression and gene status were retrospectively analyzed by immunocytochemistry and fluorescence in situ hybridization, respectively.A median of 14 courses of cetuximab (range 5-54) were infused. Skin toxicity was the main adverse event. Cetuximab provides a CBR in 50% (95% CL, 31 to 69%) of cases. None tumor sample showed EGFR gene amplification and an increased EGFR copy number was observed in 12% of samples, all ACC. Skin rash >= G2, EGFR overexpression and EGFR copy number were not statistically correlated to CB.In RMSGCs further evaluations of EGFR targeting agents are advisable and should take place by appropriate tumor biological selection, differentiating ACC from non-ACC. (C) 2008 Elsevier Ltd. All rights reserved.