2014年ASCO大会上的结
研究详情：
来自OPUS研究的患者提供KRAS外显子wt肿瘤，利用BEAMing技术（5%灵敏度临界作为分析）对4个额外KRAS密码子（外显子3和4）和6个NRAS密码子（外显子2，3和4）的26个基因突变（新RAS）进行筛查。根据RAS基因突变状态（KRAS外显子3+新RAS），对预后进行评估。
研究结果：
179例KRAS外显子2野生型肿瘤患者中有118例（66%）的基因状态可评估。新RAS基因突变在31/118（66%）例患者可检测到。那些RAS wt肿瘤患者中，通过将西妥昔单抗添加到FOLFOX4方案（表）中，响应得到明显提高。由于患者数量较低，那些新RAS肿瘤基因突变患者的治疗效果不能被确切地评估。在任何肿瘤RAS基因突变（KRAS外显子2+新RAS）患者中，没有观察到将西妥昔单抗添加到FOLFOX4方案中的获益，伴有一个较差预后的明显趋势。
表
缩写：cet，西妥昔单抗；HR，风险比；mt，突变型；*RAS评估人群，N=118；†OPUS KRAS评估人群亚群，N=315； ‡Cochran-Mantel-Haenszel；§对数秩检验
研究结论：
含有任何激活RAS基因突变的mCRC患者不太可能从西妥昔单抗+ FOLFOX4治疗方案中获益。限制给肿瘤野生型所有基因位点患者使用西妥昔单抗，可能有助于进一步的治疗调整以最大限度的提高患者利益。临床试验信息：NCT00125034。
医脉通整理报道，转载请注明出处。
会议专题》》》2014年ASCO年会专题报道
阅读摘要原文
Treatmentoutcome according to tumor RAS mutationstatus in OPUS study patients with metastatic colorectal cancer (mCRC)randomized to FOLFOX4 with/without cetuximab.（Abstract3505）
Authors: Carsten Bokemeyer,Claus-Henning Kohne,Fortunato Ciardiello,et al.
Session Type: Oral Abstract Session
Background: The addition ofcetuximab to FOLFOX4 significantly improved progression-free survival andresponse in the first-line treatment of patients (pts) with KRAS codon 12/13(hereinafter exon 2) wild-type (wt) mCRC. Pts with KRASexon 2 tumormutations showed no such cetuximab benefit, with a trend for worseoutcome.
Methods: Available KRAS exon 2 wttumors from OPUS study pts were screened for 26 mutations (new RAS) in 4additional KRAS codons(exons 3 and 4) and 6NRAS codons (exons 2, 3 and 4) usingBEAMing technology (5% sensitivity cutoff selected for analysis). Outcome wasassessed according to RAS mutation status (KRAS exon 2 +new RAS).
Results: Mutation statuswas evaluable in 118/179 (66%) pts with KRAS exon 2 wt tumors. New RAS mutationswere detected in 31/118 (26%) pts. In those with RAS wt tumors,response was significantly improved by the addition of cetuximab to FOLFOX4(Table). The treatment effect for those with new RAS tumormutations could not be definitively assessed due to low pt numbers. In pts withany tumor RAS mutation (KRAS exon 2+new RAS), no benefit from the addition of cetuximab to FOLFOX4was seen, with a clear trend for worse outcome.
Conclusions: Pts with mCRCharboring any activating RAS mutation areunlikely to benefit from the addition of cetuximab to FOLFOX4. Restrictingcetuximab administration to pts with tumors wt at all such loci might helpfurther tailoring of therapy to maximize pt benefit. Clinical trialinformation: NCT00125034.
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