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由ARID1A和PIK3CA突变引起的卵巢透明细胞癌小鼠模型的全基因组基因表达谱分析表明炎症细胞因子信号传导发挥了作用。

Global gene expression profiling of a mouse model of ovarian clear cell carcinoma caused by ARID1A and PIK3CA mutations implicates a role for inflammatory cytokine signaling.

作者信息

Chandler Ronald L, Raab Jesse R, Vernon Mike, Magnuson Terry, Schisler Jonathan C

机构信息

Department of Genetics, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA ; Lineberger Comprehensive Cancer Center, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.

Functional Genomics Core, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.

出版信息

Genom Data. 2015 Jul 14;5:329-32. doi: 10.1016/j.gdata.2015.06.027. eCollection 2015 Sep.

Abstract

Ovarian clear-cell carcinoma (OCCC) is an aggressive form of epithelial ovarian cancer (EOC). OCCC represents 5-25% of all EOC incidences and is the second leading cause of death from ovarian cancer (Glasspool and McNeish, 2013) [1]. A recent publication by Chandler et al. reported the first mouse model of OCCC that resembles human OCCC both genetically and histologically by inducing a localized deletion of ARID1A and the expression of the PIK3CA(H1047R) substitution mutation (Chandler et al., 2015) [2]. We utilized Affymetrix Mouse Gene 2.1 ST arrays for the global gene expression profiling of mouse primary OCCC tumor samples and animal-matched normal ovaries to identify cancer-dependent gene expression. We describe the approach used to generate the differentially expressed genes from the publicly available data deposited at the Gene Expression Omnibus (GEO) database under the accession number GSE57380. These data were used in cross-species comparisons to publically available human OCCC gene expression data and allowed the identification of coordinately regulated genes in both mouse and human OCCC and supportive of a role for inflammatory cytokine signaling in OCCC pathogenesis (Chandler et al., 2015) [2].

摘要

卵巢透明细胞癌(OCCC)是上皮性卵巢癌(EOC)的一种侵袭性形式。OCCC占所有EOC发病率的5%-25%,是卵巢癌死亡的第二大主要原因(格拉斯普尔和麦克尼什,2013年)[1]。钱德勒等人最近发表的一篇论文报道了首个OCCC小鼠模型,该模型通过诱导ARID1A的局部缺失和PIK3CA(H1047R)替代突变的表达,在基因和组织学上都类似于人类OCCC(钱德勒等人,2015年)[2]。我们利用Affymetrix小鼠基因2.1 ST阵列对小鼠原发性OCCC肿瘤样本和动物匹配的正常卵巢进行全基因组表达谱分析,以确定癌症相关的基因表达。我们描述了从基因表达综合数据库(GEO)中登录号为GSE57380的公开可用数据中生成差异表达基因的方法。这些数据用于与公开可用的人类OCCC基因表达数据进行跨物种比较,从而能够鉴定出小鼠和人类OCCC中协同调控的基因,并支持炎症细胞因子信号在OCCC发病机制中的作用(钱德勒等人,2015年)[2]。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d27/4583684/033014a62631/gr1.jpg

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