Kimchi Erik T, Posner Mitchell C, Park James O, Darga Thomas E, Kocherginsky Masha, Karrison Theodore, Hart John, Smith Kerrington D, Mezhir James J, Weichselbaum Ralph R, Khodarev Nikolai N
Department of Surgery, University of Chicago, Chicago, IL 60637, USA.
Cancer Res. 2005 Apr 15;65(8):3146-54. doi: 10.1158/0008-5472.CAN-04-2490.
We did expressional profiling on 24 paired samples of normal esophageal epithelium, Barrett's metaplasia, and esophageal adenocarcinomas. Matching tissue samples representing the three different histologic types were obtained from each patient undergoing esophagectomy for adenocarcinoma. Our analysis compared the molecular changes accompanying the transformation of normal squamous epithelium with Barrett's esophagus and adenocarcinoma in individual patients rather than in a random cohort. We tested the hypothesis that expressional profiling may reveal gene sets that can be used as molecular markers of progression from normal esophageal epithelium to Barrett's esophagus and adenocarcinoma. Expressional profiling was done using U133A GeneChip (Affymetrix), which represent approximately two thirds of the human genome. The final selection of 214 genes permitted the discrimination of differential gene expression of normal esophageal squamous epithelium, Barrett's esophagus, and adenocarcinoma using two-dimensional hierarchical clustering of selected genes. These data indicate that transformation of Barrett's esophagus to adenocarcinoma is associated with suppression of the genes involved in epidermal differentiation, including genes in 1q21 loci and corresponding to the epidermal differentiation complex. Correlation analysis of genes concordantly expressed in Barrett's esophagus and adenocarcinoma revealed 21 genes that represent potential genetic markers of disease progression and pharmacologic targets for treatment intervention. PCR analysis of genes selected based on DNA array experiments revealed that estimation of the ratios of GATA6 to SPRR3 allows discrimination among normal esophageal epithelium, Barrett's dysplasia, and adenocarcinoma.
我们对24对正常食管上皮、巴雷特化生和食管腺癌样本进行了表达谱分析。从每位接受腺癌食管切除术的患者身上获取了代表三种不同组织学类型的匹配组织样本。我们的分析比较了个体患者而非随机队列中正常鳞状上皮向巴雷特食管和腺癌转变过程中伴随的分子变化。我们检验了这样一个假设,即表达谱分析可能揭示可作为从正常食管上皮向巴雷特食管和腺癌进展的分子标志物的基因集。使用代表约三分之二人基因组的U133A基因芯片(Affymetrix)进行表达谱分析。通过对选定基因进行二维层次聚类,最终选择的214个基因能够区分正常食管鳞状上皮、巴雷特食管和腺癌的差异基因表达。这些数据表明,巴雷特食管向腺癌的转变与参与表皮分化的基因的抑制有关,包括1q21位点的基因以及对应于表皮分化复合体的基因。对在巴雷特食管和腺癌中协同表达的基因进行的相关性分析揭示了21个基因,这些基因代表了疾病进展的潜在遗传标志物和治疗干预的药理学靶点。基于DNA阵列实验选择的基因的PCR分析表明,GATA6与SPRR3的比率估计能够区分正常食管上皮、巴雷特发育异常和腺癌。