Campagna Domenico, Cope Leslie, Lakkur Sindhu S, Henderson Clark, Laheru Daniel, Iacobuzio-Donahue Christine A
Departments of Pathology, The Johns Hopkins Hospital, Baltimore, Maryland, USA.
Int J Clin Exp Pathol. 2008 Jan 1;1(1):32-43.
Few studies have addressed the expression profiles associated with progression of pancreatic cancer to advanced disease. Towards this end, we performed expression profiling of a series of normal pancreas, pancreatitis and cancer tissues representing early stage resected pancreatic cancers (stages pT2/T3), late stage unresectable cancers (stage pT4) and matched metastases to a variety of organ sites. Microarray data was analyzed using linear modeling of microarray data (LIMMA), and differentially expressed genes were subjected to Gene Set Enrichment Analysis (GSEA). While robust differences were found in primary cancers as compared to normal pancreatic tissues, no differences were found between primary cancers and metastases, whether using matched or unmatched samples. When resected pancreatic cancers were specifically compared to advanced pancreatic cancers, significant differences in gene expression were found associated with growth at the primary site. These differentially expressed genes were most prominent in gene classes that related to MAPK and Wnt pathway, metabolism, immune regulation, cell-cell and cell-matrix interactions within the infiltrating carcinoma. One candidate upregulated gene (MXI1) was validated as having increased expression in advanced stage (T4) carcinomas by real-time PCR (p<0.05) and immunolabeling (p<0.003). We conclude that in addition to the robust changes in expression that accompany pancreatic carcinogenesis additional specific changes occur in association with growth at the primary site. By contrast, metastatic spread is not accompanied by reproducible changes in gene expression. These findings add to our understanding of pancreatic cancer and offer new topics for investigation into the aggressive nature of this deadly tumor type.
很少有研究探讨与胰腺癌进展至晚期疾病相关的表达谱。为此,我们对一系列正常胰腺、胰腺炎和癌症组织进行了表达谱分析,这些组织分别代表早期切除的胰腺癌(pT2/T3期)、晚期不可切除的癌症(pT4期)以及转移至各种器官部位的匹配转移灶。使用微阵列数据的线性建模(LIMMA)分析微阵列数据,并对差异表达基因进行基因集富集分析(GSEA)。与正常胰腺组织相比,原发性癌症中发现了显著差异,但无论是使用匹配还是不匹配的样本,原发性癌症与转移灶之间均未发现差异。当将切除的胰腺癌与晚期胰腺癌进行特异性比较时,发现基因表达存在显著差异,这些差异与原发部位的生长相关。这些差异表达基因在与丝裂原活化蛋白激酶(MAPK)和Wnt信号通路、代谢、免疫调节、浸润癌中的细胞间和细胞与基质相互作用相关的基因类别中最为突出。一个上调的候选基因(MXI1)通过实时聚合酶链反应(p<0.05)和免疫标记(p<0.003)验证在晚期(T4)癌中表达增加。我们得出结论,除了胰腺癌发生过程中伴随的强大表达变化外,与原发部位生长相关还会发生其他特定变化。相比之下,转移扩散并不伴随着基因表达的可重复变化。这些发现增进了我们对胰腺癌的理解,并为研究这种致命肿瘤类型的侵袭性提供了新的研究课题。