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剖析显微切割的上皮组织和基质,以建立适应协变量的宫颈癌发生基因组特征模型。

Profiling microdissected epithelium and stroma to model genomic signatures for cervical carcinogenesis accommodating for covariates.

作者信息

Gius David, Funk Margo C, Chuang Eric Y, Feng Sheng, Huettner Phyllis C, Nguyen Loan, Bradbury C Matthew, Mishra Mark, Gao Shuping, Buttin Barbara M, Cohn David E, Powell Matthew A, Horowitz Neil S, Whitcomb Bradford P, Rader Janet S

机构信息

Radiation Oncology Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland 20892, USA.

出版信息

Cancer Res. 2007 Aug 1;67(15):7113-23. doi: 10.1158/0008-5472.CAN-07-0260.

Abstract

This study is the first comprehensive, integrated approach to examine grade-specific changes in gene expression along the entire neoplastic spectrum of cervical intraepithelial neoplasia (CIN) in the process of cervical carcinogenesis. This was accomplished by identifying gene expression signatures of disease progression using cDNA microarrays to analyze RNA from laser-captured microdissected epithelium and underlying stroma from normal cervix, graded CINs, cancer, and patient-matched normal cervical tissues. A separate set of samples were subsequently validated using a linear mixed model that is ideal to control for interpatient gene expression profile variation, such as age and race. These validated genes were ultimately used to propose a genomically based model of the early events in cervical neoplastic transformation. In this model, the CIN 1 transition coincides with a proproliferative/immunosuppression gene signature in the epithelium that probably represents the epithelial response to human papillomavirus infection. The CIN 2 transition coincides with a proangiogenic signature, suggesting a cooperative signaling interaction between stroma and tumor cells. Finally, the CIN 3 and squamous cell carcinoma antigen transition coincide with a proinvasive gene signature that may be a response to epithelial tumor cell overcrowding. This work strongly suggests that premalignant cells experience a series of microenvironmental stresses at the epithelium/stroma cell interface that must be overcome to progress into a transformed phenotype and identifies the order of these events in vivo and their association with specific CIN transitions.

摘要

本研究是首次采用全面、综合的方法,在宫颈癌发生过程中,沿着宫颈上皮内瘤变(CIN)的整个肿瘤谱检查特定分级的基因表达变化。这是通过使用cDNA微阵列分析来自激光捕获显微切割的正常宫颈上皮及下方基质、分级CIN、癌症以及患者匹配的正常宫颈组织的RNA,来确定疾病进展的基因表达特征而实现的。随后,使用线性混合模型对另一组样本进行验证,该模型非常适合控制患者间基因表达谱的差异,如年龄和种族。这些经过验证的基因最终被用于提出一个基于基因组的宫颈肿瘤转化早期事件模型。在这个模型中,CIN 1转变与上皮细胞中促增殖/免疫抑制基因特征相吻合,这可能代表了上皮细胞对人乳头瘤病毒感染的反应。CIN 2转变与促血管生成特征相吻合,表明基质与肿瘤细胞之间存在协同信号相互作用。最后,CIN 3和鳞状细胞癌抗原转变与促侵袭基因特征相吻合,这可能是对上皮肿瘤细胞过度拥挤的一种反应。这项工作有力地表明,癌前细胞在上皮/基质细胞界面经历了一系列微环境应激,要进展为转化表型就必须克服这些应激,并确定了这些事件在体内的顺序及其与特定CIN转变的关联。

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