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首页> 美国卫生研究院文献>Wiley-Blackwell Online Open >HER2 overexpression and amplification as a potential therapeutic target in colorectal cancer: analysis of 3256 patients enrolled in the QUASAR FOCUS and PICCOLO colorectal cancer trials
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HER2 overexpression and amplification as a potential therapeutic target in colorectal cancer: analysis of 3256 patients enrolled in the QUASAR FOCUS and PICCOLO colorectal cancer trials

机译：HER2过表达和扩增是结直肠癌的潜在治疗靶点：对QUASARFOCUS和PICCOLO结直肠癌试验的3256名患者的分析

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摘要

HER2 overexpression/amplification is linked to trastuzumab response in breast/gastric cancers. One suggested anti‐EGFR resistance mechanism in colorectal cancer (CRC) is aberrant MEK–AKT pathway activation through HER2 up‐regulation. We assessed HER2‐amplification/overexpression in stage II–III and IV CRC patients, assessing relationships to KRAS/BRAF and outcome. Pathological material was obtained from 1914 patients in the QUASAR stage II–III trial and 1342 patients in stage IV trials (FOCUS and PICCOLO). Tissue microarrays were created for HER2 immunohistochemistry. style="italic-in-any-context"> style="fixed-case">HER2‐amplification was assessed using style="fixed-case">FISH and copy number variation. style="italic-in-any-context"> style="fixed-case">KRAS/ style="italic-in-any-context"> style="fixed-case">BRAF mutation status was assessed by pyrosequencing. Progression‐free survival ( style="fixed-case">PFS) and overall survival ( style="fixed-case">OS) data were obtained for style="fixed-case">FOCUS/ style="fixed-case">PICCOLO and recurrence and mortality for style="fixed-case">QUASAR; 29/1342 (2.2%) stage style="fixed-case">IV and 25/1914 (1.3%) stage style="fixed-case">II–III tumours showed style="fixed-case">HER2 protein overexpression. Of the style="fixed-case">HER2‐overexpressing cases, 27/28 (96.4%) stage style="fixed-case">IV tumours and 20/24 (83.3%) stage style="fixed-case">II–III tumours demonstrated style="italic-in-any-context"> style="fixed-case">HER2 amplification by style="fixed-case">FISH; 41/47 (87.2%) also showed copy number gains. style="fixed-case">HER2‐overexpression was associated with style="italic-in-any-context"> style="fixed-case">KRAS/ style="italic-in-any-context"> style="fixed-case">BRAF wild‐type ( style="fixed-case">WT) status at all stages: in 5.2% style="fixed-case">WT versus 1.0% mutated tumours ( style="italic-in-any-context">p < 0.0001) in stage style="fixed-case">IV and 2.1% versus 0.2% in stage style="fixed-case">II–III tumours ( style="italic-in-any-context">p = 0.01), respectively. style="fixed-case">HER2 was not associated with style="fixed-case">OS or style="fixed-case">PFS. At stage style="fixed-case">II–III, there was no significant correlation between style="fixed-case">HER2 overexpression and style="fixed-case">5FU/ style="fixed-case">FA response. A higher proportion of style="fixed-case">HER2‐overexpressing cases experienced recurrence, but the difference was not significant. style="fixed-case">HER2‐amplification/overexpression is identifiable by immunohistochemistry, occurring infrequently in stage style="fixed-case">II–III CRC, rising in stage style="fixed-case">IV and further in style="italic-in-any-context"> style="fixed-case">KRAS/ style="italic-in-any-context"> style="fixed-case">BRAF style="fixed-case">WT tumours. The value of style="fixed-case">HER2‐targeted therapy in patients with style="italic-in-any-context">HER2‐amplified style="fixed-case">CRC must be tested in a clinical trial. © 2015 The Authors. style="italic-in-any-context">Journal of Pathology published by John Wiley & Sons Ltd on behalf of Pathological Society of Great Britain and Ireland.
机译：HER2的过表达/扩增与曲妥珠单抗在乳腺癌/胃癌中的反应有关。在结直肠癌（CRC）中，一种建议的抗EGFR耐药机制是通过HER2上调来异常激活MEK-AKT途径。我们评估了II–III和IV期CRC患者的HER2扩增/过表达，评估了与KRAS / BRAF和结局的关系。 QUASAR II-III试验的1914例患者和IV阶段试验的1342例患者（FOCUS和PICCOLO）获得了病理材料。创建用于HER2免疫组织化学的组织微阵列。 style =“ italic-in-any-context”> style =“ fixed-case”> HER2 -使用 style =“ fixed-case”> FISH < / span>，然后复制编号。 style =“ italic-in-any-context”> style =“ fixed-case”> KRAS / style =“ italic-in-any-context”> 通过焦磷酸测序法评估了BRAF 突变状态。获得了 style =“的无进展生存期（ style =” fixed-case“> PFS ）和总生存期（ style =” fixed-case“> OS ）数据。 fixed-case“> FOCUS / style =” fixed-case“> PICCOLO 和 style =” fixed-case“> QUASAR 的复发率和死亡率； 29/1342（2.2％）期 style =“ fixed-case”> IV 和25/1914（1.3％）期 style =“ fixed-case”> II–III 肿瘤显示 style =“ fixed-case”> HER2 蛋白过表达。在 style =“ fixed-case”> HER2 -过表达的病例中，有27/28（96.4％）分期的 style =“ fixed-case”> IV 肿瘤和20/24（ 83.3％）分期 style =“ fixed-case”> II-III 肿瘤显示 style =“ italic-in-any-context”> style =“ fixed-case”> HER2 通过 style =“ fixed-case”> FISH 放大； 41/47（87.2％）也显示了副本数的增长。 style =“ fixed-case”> HER2 -过表达与 style =“ italic-in-any-context”> style =“ fixed-case”> KRAS < / span> / style =“ italic-in-any-context”> style =“ fixed-case”> BRAF 野生型（ style =“ fixed-case” > WT ）状态：在5.2％ style =“ fixed-case”> WT 和1.0％突变的肿瘤中（ style =“ italic-in-any-context”>在 style =“ fixed-case”> IV 阶段中，p / span> 0.0001）和2.1％相对于在 style =“ fixed-case”> II-III 阶段中为0.2％肿瘤（ style =“ italic-in-any-context”> p = 0.01）。 style =“ fixed-case”> HER2 与 style =“ fixed-case”> OS 或 style =“ fixed-case”> PFS 没有关联。在阶段 style =“ fixed-case”> II-III ， style =“ fixed-case”> HER2 过表达与 style =“ fixed- case“> 5FU / style =” fixed-case“> FA 响应。 style =“ fixed-case”> HER2 -过表达的病例中有较高比例复发，但差异不显着。 style =“ fixed-case”> HER2 -扩增/过表达可通过免疫组织化学鉴定，很少发生在 style =“ fixed-case”> II-III CRC 阶段， style =“ fixed-case”> IV ，并进一步 style =“ italic-in-any-context”> style =“ fixed-case”> KRAS / style =“ italic-in-any-context”> style =“ fixed-case”> BRAF style =“ fixed-case”> WT 肿瘤。 style =“ fixed-case”> HER2 靶向治疗在 style =“ italic-in-any-context”> HER2 -放大的 style =“固定病例“> CRC 必须在临床试验中进行测试。 ©2015作者。约翰·威利父子有限公司（John Wiley＆Sons Ltd）代表大不列颠及爱尔兰病理学会出版的《病理学杂志》（span style =“ italic-in-any-context”> Journal of Pathology）。

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