Gene expression in colon cancer: A focus on tumor site and molecular phenotype.
Gene expression in colon cancer: A focus on tumor site and molecular phenotype.
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DOI：
10.1002/gcc.22265
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发表时间：
2015-09
期刊：
影响因子：
--
通讯作者：
Herrick JS
中科院分区：
文献类型：
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作者：
Slattery ML;Pellatt DF;Mullany LE;Wolff RK;Herrick JS
与非肿瘤结肠组织样本相比，肿瘤中有数百至数千个基因差异表达。我们评估了基因表达模式，以更好地了解肿瘤部位和肿瘤分子表型在结肠癌中的差异。我们分析了来自175名结肠癌患者的肿瘤/正常配对样本的RNA-seq数据。我们实施了一个交叉验证策略与非参数测试，以确定基因，显示不同的表达特征相关的配对肿瘤/非肿瘤组织在近端和远端结肠网站和肿瘤分子表型，即TP 53，KRAS，CpG岛甲基化表型（CIMP），和微卫星不稳定性（MSI）。我们使用Ingenuity Pathway Analysis（IPA）来确定数据中与失调基因相关的网络。在两个验证组中，肿瘤亚位点（116个基因）、CIMP高与CIMP低（79个基因）、MSI与微卫星稳定（MSS）（49个基因）、TP 53突变与未突变（17个基因）和KRAS突变与未突变（1个基因）之间的基因表达特征在0.01水平上显示出显著差异。CIMP高和MSI肿瘤的失调基因通常下调。与CIMP高和MSI肿瘤相反，TP 53中失调的基因可能上调。ERK 1、WNT、生长因子和炎症相关因子是CIMP和MSI IPA网络的焦点。MUC家族基因呈上调的MSI网络。许多基因在近端和远端肿瘤、非肿瘤近端和远端组织以及肿瘤分子表型之间表现出表达差异。去调节的粘蛋白基因似乎在MSI肿瘤中起重要作用。
Hundreds to thousands of genes are differentially expressed in tumors when compared to nontumor colonic tissue samples. We evaluated gene expression patterns to better understand differences in colon cancer by tumor site and tumor molecular phenotype. We analyzed RNA-seq data from tumor/normal paired samples from 175 colon cancer patients. We implemented a cross validation strategy with nonparametric tests to identify genes which displayed varying expression characteristics related to paired tumor/nontumor tissue across proximal and distal colon sites and by tumor molecular phenotypes, that is, TP53, KRAS, CpG Island Methylator Phenotype (CIMP), and microsatellite instability (MSI). We used Ingenuity Pathway Analysis (IPA) to determine networks associated with deregulated genes in our data. Genes showed significant differences in expression characteristics at the 0.01 level in both validation groups between tumor subsite (116 genes), CIMP high versus CIMP low (79 genes), MSI versus microsatellite stable (MSS) (49 genes), TP53-mutated versus not mutated (17genes), and KRAS-mutated versus not mutated (1 gene). Deregulated genes for CIMP high and MSI tumors were often down-regulated. In contrast to CIMP high and MSI tumors, genes that were deregulated in TP53 were likely to be up-regulated. ERK1, WNT, growth factors and inflammation-related factors were focal points of both CIMP and MSI IPA networks. The MUC family of genes was up-regulated MSI networks. Numerous genes showed differences in expression between proximal and distal tumors, nontumor proximal and distal tissue, and tumor molecular phenotype. Deregulated mucin genes appear to play an important role in MSI tumors.
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影响因子：
--
作者：
Pastrello C;Santarosa M;Fornasarig M;Sigon R;Perin T;Giannini G;Boiocchi M;Viel A
通讯作者：
Viel A
影响因子：
3.7
作者：
Sanz-Pamplona R;Berenguer A;Cordero D;Riccadonna S;Solé X;Crous-Bou M;Guinó E;Sanjuan X;Biondo S;Soriano A;Jurman G;Capella G;Furlanello C;Moreno V
通讯作者：
Moreno V
影响因子：
29.4
作者：
Samowitz, WS;Curtin, K;Slattery, ML
通讯作者：
Slattery, ML
影响因子：
8.8
作者：
Belshaw, N. J.;Elliott, G. O.;Johnson, I. T.
通讯作者：
Johnson, I. T.
DOI：
10.1093/jnci/92.22.1831
发表时间：
2000-11-15
期刊：
JOURNAL OF THE NATIONAL CANCER INSTITUTE
影响因子：
--
作者：
Slattery, ML;Curtin, K;Samowitz, WS
通讯作者：
Samowitz, WS